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128 publications mentioning mmu-mir-27b (showing top 100)

Open access articles that are associated with the species Mus musculus and mention the gene name mir-27b. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 249
Other miRNAs from this paper: mmu-mir-23b, mmu-mir-23a, mmu-mir-27a
In contrast with published studies, PPARγ expression in cultured macrophages was only modestly affected by mir-27b mimicry, however, it was significantly upregulated by miR-27b inhibitor. [score:8]
We offer targeting the miR-27b-regulated pathways with miR-27b -based drugs for the treatment of cardiovascular disease. [score:6]
Moreover, hepatic miR-27b is downregulated and its targets elevated in mouse mo dels of dyslipidemia/atherosclerosis [54]. [score:6]
miR-27 effects in the heart are context -dependent: although it is necessary for ventricular maturation, targeted overexpression in cardiomyocytes causes hypertrophy and dysfunction during development. [score:6]
However, miR-27b is also targeted by TGF-β [52] and in vivo overexpression results suggest potential harmful effects in adult heart. [score:5]
In the endothelial cells, Notch signaling interferes with tip cell fate [35]: therefore suppression of Dll4 with miR-27b mimic should allow tip cell fate and increases vascular sprouting, and miR-27b interference should augment Dll4 and inhibit vascular sprouts. [score:5]
Together, our findings demonstrate potential utility of manipulating miR-27b levels in cardiovascular disease and cancer and confirm its targets as Dll4/Notch axis, PPARγ and its downstream effectors. [score:5]
miR-27b inhibitor suppresses cancer growth and angiogenesis. [score:5]
Here, we assessed the therapeutic potential of miR-27b mimics and inhibitors in rodent mo dels of ischemic disease and cancer. [score:5]
NT, no treatment; NC, negative control; 27b(M), miR-27b mimic; 27b(I), miR-27b inhibitor Previous studies from our group implicated the suppression of Notch ligand, Dll4 in the pro-angiogenic action of miR-27b [26]. [score:5]
We have ascertained the appropriate increase and decrease of mature miR-27b levels in the target tissues of animals treated with miR-27b mimic and inhibitor, respectively, by real-time PCR (Additional file 1: Figures S2 and S5). [score:5]
In contrast, co-localization analysis with the vascular endothelial marker, CD31, showed a significant reduction of Dll4 specifically on tumor vasculature caused by miR-27b mimic; in agreement, miR-27b inhibitor clearly augmented Dll4 expression by the tumor vasculature (Fig.   5f, g). [score:5]
Indeed, miR-27b silencing in pressure overload mo del attenuated hypertrophy, by restoring the expression of its other target, PPARγ [51]. [score:5]
The role of miR-27b in the regulation of angiogenesis was discovered by several groups [26– 28] and its angiogenesis-related targets identified as Dll4 [26], Sema 6A and Sprouty-2 [26, 28, 46]. [score:4]
It is unclear, however, whether long-term application of miR-27b and/or other miRNA from this cluster could be harmful for cardiomyocytes and require additional targeting to the vascular endothelium, or if there would be long-term beneficial effects on PAD via attenuated lipid metabolism and fat tissue development. [score:4]
miR-27b is also upregulated in glioma where it promotes tumor growth and invasion. [score:4]
On the other hand, the 23/27b cluster and miR-27b are downregulated and ascribed anti-tumorigenic roles in the cell lines derived from the tumors of bladder, prostate and colon [39, 61, 65, 66]. [score:4]
We have shown previously that miR-27b promotes capillary sprouting and endothelial tip fate by suppressing the Notch ligand, Delta-like ligand 4 (Dll4) and the negative regulator of branching, Sprouty-2 (Spry-2) [26]. [score:4]
The difference in the regulation of Dll4 in the tumor cells and vascular endothelium could be due to the tissue context, where miR-27b could cooperate with RNA binding protein(s), such as HuR [36– 38] causing mRNA stabilization and translational activation. [score:4]
Statistical significance was assessed by Wilcoxon Signed Rank test, as aboveIn LPS -treated macrophages, miR-27b was previously shown to target PPARγ and alter the downstream regulation of inflammatory cytokines [39]. [score:4]
Statistical significance was assessed by Wilcoxon Signed Rank test, as above In LPS -treated macrophages, miR-27b was previously shown to target PPARγ and alter the downstream regulation of inflammatory cytokines [39]. [score:4]
Despite significant recent advances, therapeutic potential of miR-27b in cardiovascular disease and its effects in adult heart remain unexplored. [score:3]
Here, we provide experimental evidence that therapeutic manipulation of miR-27b can be beneficial in angiogenesis -dependent disease. [score:3]
We have used a number of mo dels to demonstrate the effects of miR-27b mimicry and inhibition in vivo, including subcutaneous, mouse mo dels of hind limb ischemia and myocardial infarction and subcutaneous Lewis Lung carcinoma. [score:3]
P values are shownIn subcutaneous LLC tumors, miR-27b had disparate effects on the total and vascular Dll4 expression. [score:3]
Limited local application of miR-27b mimic was sufficient to restore angiogenesis and improve tissue function in two mo dels of ischemic disease, hind limb ischemia, which mimics CLI, and coronary artery ligation, a MI mo del. [score:3]
For every 2 × 10 [6] 30 nM miR-27b mimic, inhibitor, NC RNAi or 2 μg GFP plasmid (transfection control) were in added. [score:3]
miRNA miR-27b Therapeutic angiogenesis Ischemia Cardiovascular Cancer Angiogenesis is a tightly regulated process, which is critical for organ development and tissue homeostasis in adults [1]. [score:3]
MirVana brand miRNA mimics (double-stranded oligonucleotides, with star strand inactivated by chemical modifications for maximal specificity) included negative control (NC) and mmu-miR-27b and miR-27b inhibitor (antagomir). [score:3]
Our study demonstrates the utility of manipulating miR-27b levels in the treatment of cardiovascular disease and cancer. [score:3]
These findings suggest that miR-27 inhibitors may have beneficial effects in cancer setting by blocking the recruitment and activation of tumor -associated macrophages. [score:3]
Note decreased MVD when miR-27b is inhibited, 27b(I). [score:3]
Our findings suggest that miR-27b has different effects on tumor cells and the cells of tumor microenvironment as is evidenced by its disparate effect on Dll4 expression in the tumor and tumor vasculature. [score:3]
P values are shown In subcutaneous LLC tumors, miR-27b had disparate effects on the total and vascular Dll4 expression. [score:3]
Spry-2, another known target of miR-27b was not significantly altered (Additional file 1: Figure S4). [score:3]
Mice with LLC tumors (5–7 mm diameter) were randomized into groups (n = 5) and treated with intraperitoneal injections of NC, miR-27b mimic or inhibitor, formulated as above (100 μg/100 μl/mouse). [score:3]
In addition, local use of oligonucleotide mimics of miR-27b facilitates the recruitment of endogenous bone marrow-derived stem cells to the newly forming vasculature at the target site. [score:3]
PPARγ (e), a miR-27b target, and inflammatory chemokines IL-10 (f) and IL-12 (g) were assessed by real-time RT-PCR and normalized against untreated control (NT no treatment). [score:3]
Together, our results demonstrate potential utility of manipulating miR-27b levels in the treatment of cardiovascular disease and cancer as well as associated inflammatory processes and indicate several molecular mechanisms involved. [score:3]
Five-μm crosswise tissue sections of calf muscle or tumor tissue were stained for Dll4, a miR-27b target (green). [score:3]
When tumors reached 5–6 mm in diameter, the animals were treated every 2 days with intraperitoneal injections of NC RNAi, miR-27b mimic 27b(M) or inhibitor, 27b(I) at 100 μg per mouse per injection (n = 5). [score:3]
Systemic treatment with miR-27b inhibitor, 27b(I) at 5 mg/kg caused a significant reduction of tumor weight at the endpoint (Fig.   4a- c, 1: Figure S5). [score:3]
In addition, miR-27b is decreased in differentiating adipocytes and inhibits their proliferation and accumulation via PPARγ/RXRα controlled pathways [55, 56]. [score:3]
When tumors reached 5 mm in diameter, animals were randomized into groups (n = 5) and treated with miR-27b mimic, inhibitor and negative control complexes prepared in sterile 5 % glucose using in vivo-jetPEI (PolyPlus Transfection, France). [score:3]
We therefore examined the effect of miR-27b inhibitor on tumor angiogenesis and associated growth rates. [score:3]
Others have shown that miR-27b also inhibits Spry-2 and repulsive signaling by Semaphorin 6A [27, 28]. [score:3]
Our findings suggest that the use of miR-27b inhibitors may be feasible in the context of personalized of cancer patients care. [score:3]
miR-27b manipulations alter Dll4 expression in ischemic and tumor tissue. [score:3]
In cancer, the role of miR-27b is controversial, with studies lending support to its tumor-promoting and tumor-suppressive roles. [score:3]
miR-27b was previously implicated in the regulation of macrophage responses [39]. [score:2]
This function of miR-27b could indirectly benefit PAD patients. [score:2]
Hepatic miR-27b is increased in response to hyperlipidemia and, in turn, regulates several key genes in control of lipid metabolism (Angptl3, Gpam) [54]. [score:2]
In agreement, simultaneous knockdown of miR-23 and miR-27b in the miR-23/27/24 cluster attenuated neonatal retinal angiogenesis as well as laser -induced choroidal neovascularization [28]. [score:2]
Interestingly, miR-27b deficit could contribute to PAD indirectly, via lipid metabolism. [score:2]
miR-27b has been identified as a classical oncomir in cell -based assays [59] and its elevated expression is associated with poor prognosis, chemoresistance and metastasis in carcinomas of the ovary and the breast [60] and in castrate-resistant prostate cancer [61]. [score:2]
In both mo dels, miR-27b mimic clearly decreased macrophage recruitment to the site of hypoxic injury. [score:1]
In our short-term study, we observed increased vascularization of the muscles of the heart and extremities subjected to ischemic stress, concomitant with preserved tissue integrity and function, suggestive of the therapeutic utility of miR-27b for acute treatment of critical limb ischemia and myocardial infarction. [score:1]
Thus the role of miR-27b in cancer progression is likely context -dependent. [score:1]
We therefore analyzed macrophage infiltration in ischemic and tumor tissues where miR-27b was added (mimic) or blocked (anti-miR). [score:1]
Note elevated BMDC recruitment in response to miR-27b. [score:1]
Importantly, miR-27b increased the recruitment of bone marrow derived cells (BMDCs) to the neovasculature, as was shown in mice reconstituted with GFP-tagged bone marrow. [score:1]
In HLI mo del, mice were treated by intramuscular injections of miR27b and NC mimics into the quadriceps muscle (10 μg/mouse/day, 2 injections in a total of 50 μl, via 27-gauge needle). [score:1]
IF staining showed elevated Dll4 levels in ischemic calf muscle, which was significantly reduced in the presence of miR-27b mimic (Fig.   5a, b). [score:1]
However, the lack of conversion of myeloid BMDCS to the endothelial (CD31 -positive) phenotype in vivo suggests that the majority of BMDCs recruited in response to miR-27b treatment have an accessory role where they serve as the source of pro-angiogenic and/or survival factors for the neovasculature. [score:1]
Importantly, these changes caused by miR-27b mimicry resulted in improved cardiac function, with an approximately 2-fold increase in ejection fraction over control by day 14 (Fig.   3f) and a trend towards increased fractional shortening (Fig.   3g). [score:1]
Surprisingly, treatment with anti-miR-27b also reduced the recruitment and activation of tumor -associated macrophages (TAMs). [score:1]
miR-27b mimicry promoted de novo angiogenesis and BMDC recruitment. [score:1]
Adding miR-27b mimic to the Matrigel clearly increased the number of CD31 -positive vascular structures at baseline, in the absence of pro-angiogenic VEGF and significantly augmented angiogenic response to VEGF (Fig.   1a, b). [score:1]
miR-27b preserved angiogenesis and protected tissue function in the infarcted heart. [score:1]
Improved vascularization was associated with a significant degree of tissue protection in the animals treated with miR-27b mimic. [score:1]
Importantly, miR-27b blockade also altered macrophage polarization, which was reflected by the alterations in relative abundance of the M1 and M2 markers, IL12 and IL10 (Fig.   6g, f). [score:1]
miR-27b alters macrophage infiltration in ischemic and tumor tissues. [score:1]
Studies support the role of miR-27b as cholesterol hub in the liver [53]. [score:1]
VEGF, miR-27b mimics (27b) or negative control RNAi (NC), were added to Matrigel as indicated. [score:1]
Silencing of miR-27b leads to decreased VEGF signaling and sprouting angiogenesis in vitro and in vivo (reviewed in [47]). [score:1]
In contrast, miR-27b increased the recruitment of bone marrow derived cells to the neovasculature, as was shown using mice reconstituted with fluorescence-tagged bone marrow. [score:1]
In agreement, treatment with anti-miR-27b significantly reduced tumor MVD, while miR-27b had only modest effect on already robust angiogenesis in the LLC tumors, (Fig.   4d, e). [score:1]
For the myocardial infarction (MI) mo del, miR-27b and NC mimics formulated as above were administered at the time of surgery by intracardiac injections (10 μg/mouse, two 10 μl injections), using a 10 μl Hamilton syringe with a 30-gauge needle. [score:1]
In contrast, blocking miR-27b significantly decreased vascularization and reduced growth of subcutaneous tumors and decreased BMDCs recruitment to the tumor vasculature. [score:1]
Earlier studies have demonstrated the ability of miR-27b to enhance/restore angiogenic function of the BMDCs in diabetic mice (Db/Db), causing accelerated wound healing [58]. [score:1]
Note increased vascularization in the presence of miR-27b. [score:1]
Note increased Dll4 immunostaining under ischemic conditions in animals treated with control RNAi (NC), and significant attenuation by miR-27b (27b). [score:1]
On day 0, mice were randomly assigned to groups (n = 5) and injected three times with negative control (RNAi) or miR-27b mimic (10 μg/injection/day, days 0–2; NC and 27b, respectively). [score:1]
Note a significant increase in the ejection fraction at day 14 in the hearts treated with miR-27b Angiogenesis is a rate-limiting factor in tumor progression. [score:1]
Here, we explore the possibility of therapeutic manipulation of angiogenesis by using mimicry or inactivation, as appropriate, of a pro-angiogenic microRNA, miR-27b. [score:1]
Similar decrease in Dll4 mRNA was observed by real-time PCR in cardiac tissue of mice treated with miR-27b mimic (Additional file 1: Figure S3). [score:1]
miR-27b enhanced angiogenesis and improves perfusion in the ischemic hind limb. [score:1]
Previous studies indicate that miR-27b contributes towards inflammatory processes by destabilization of PPARγ mRNA and protein [39]. [score:1]
The reduced inflammatory infiltrates in ischemic tissue may be secondary to anti-fibrotic action of miR-27b. [score:1]
Using mouse mo del of myocardial infarction due to the coronary artery ligation, we showed that miR-27b mimic had overall beneficial effects, including increased vascularization, decreased fibrosis and increased ejection fraction. [score:1]
miR-27b significantly increased recruitment of GFP -positive BMDCs to the site of VEGF -induced neovascularization (Fig.   1c, d). [score:1]
To assess the contribution of the BMDCs to the pro-angiogenic function of miR-27b we used in mice transplanted with GFP-tagged bone marrow from Tg (CAG-EGFP) 13OsbLeySopj mice. [score:1]
miR-27b significantly attenuated macrophage infiltration to the infarcted area, as was evidenced by IHC for macrophage marker, F4/80 (Fig.   6a). [score:1]
miR27b and NC mimic (20 μg/mouse) were formulated with in vivo-JetPEI (PolyPlus Transfection, France) in 5 % glucose, according to manufacturer’s instructions, and added, where indicated. [score:1]
In both mo dels, miR-27b significantly decreased inflammation as was evidenced by decreased macrophage recruitment at the site of ischemic injury. [score:1]
In a contrasting approach, blocking miR-27b by systemic administration of an anti-miR oligonucleotide significantly decreased microvacular density (MVD) and delayed the growth of highly aggressive subcutaneous tumors (Levis Lung Carcinoma, LLC-1). [score:1]
On the other hand, miR-27b altered cytokine profile of the cultured macrophages with increased IL-10 and decreased IL-12 levels suggestive of alternative (non-inflammatory) mode of activation. [score:1]
There are similar findings regarding other members of the miR-23/27/24 cluster distinct from miR-27b [57]. [score:1]
Negative control RNAi (NC) or miR-27b mimics were formulated with Jet-PEI and injected into cardiac muscle at the time of surgery (10 μg/mouse). [score:1]
We then tested whether miR-27b similarly accelerates angiogenesis in the ischemic muscle. [score:1]
After surgery, the mice received intramuscular (IM) injections of miR-27b mimic or negative control (non-silencing RNAi) for three consecutive days. [score:1]
Pro-angiogenic function of miR-27b was demonstrated in several studies [26– 28]. [score:1]
Since miR-27b itself is repressed by TGF-β [68], its reconstitution with mimics may be especially pertinent in the context of inflammation and fibrosis. [score:1]
In mouse mo del of critical limb ischemia, miR-27b mimic also improved tissue re-vascularization and perfusion. [score:1]
Treatment with miR-27b mimic significantly improved tissue vascularization, as was shown by immunofluorescence for the endothelial marker, CD31 (Fig.   2a- c). [score:1]
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2
[+] score: 153
As Mstn is a potent negative regulator of myoblast differentiation [6], we speculate that the elevated miR-27 expression may function to inhibit Mstn expression thus allowing for myogenic differentiation to proceed. [score:8]
Although it is tempting to suggest that epigenetic mechanisms (such as miR-27) could be responsible for regulating Mstn expression during differentiation, we noted that the increase in miR-27 expression during differentiation might not be enough to account for the dramatic drop in Mstn expression observed. [score:8]
Therefore, the increase in Pax7 [+] cells observed in response to over expression of miR-27 is most likely due to miR-27 -mediated inhibition of Mstn as opposed to direct regulation of Pax7 by miR-27. [score:7]
To confirm that the reduced expression of miR-27 was responsible for the elevated Mstn expression detected in Smad3 -null mice we next assessed Mstn expression between WT and Smad3 -null mice primary myoblast cultures following transfection of a miR-27b-specific mimic. [score:7]
As predicted, transfection of AntagomiR-27a or AntagomiR-27b resulted in reduced expression of miR-27a (Figure S1A) and miR-27b (Figure S1B) respectively, together with increased Mstn expression (Figure S1C). [score:5]
More recently, microRNA-27 (miR-27) has been shown to target and inhibit Mstn. [score:5]
Further support for Smad3 regulation of miR-27 is seen in published work from Sun et al, which revealed the presence of a Smad binding element in the miR-24-2/miR-23a/miR-27a cluster upstream regulatory sequence and that the Smad binding site was critical for TGF-β1 -mediated inhibition of miR-24-2/miR-23a/miR-27a [31]. [score:5]
These data are in agreement with a recently published report by Chen et al, which shows a similar increase in miR-27 expression and associated decrease in Mstn expression during myogenic differentiation [45]. [score:5]
Therefore, taken together these data suggest that posttranscriptional regulation of Mstn mRNA by miR-27 plays a critical role in controlling timely tissue-specific expression/activity of Mstn during development. [score:5]
Here we have investigated if miR-27a/b could be responsible for the increased Mstn expression observed in Smad3 -null mice; and in agreement with increased Mstn expression we find reduced miR-27a and miR-27b expression in Smad3 -null mice. [score:5]
As differentiation ensued we noted a decrease in Mstn expression, consistent with previous reports [43], [44], concomitant with a steady increase in miR-27 expression. [score:5]
Importantly, transfection of the miR-27b mimic reduced the expression of Mstn back to levels comparable to that observed in WT controls (Figure 5F), suggesting that reduced miR-27a/b expression may be responsible for the increased levels of Mstn observed in Smad3 -null mice. [score:5]
In agreement with this, we observed significantly increased expression of Mstn together with pronounced myotubular atrophy upon AntagomiR -mediated inhibition of miR-27a and miR-27b. [score:5]
More importantly, mimic -mediated over expression of miR-27b in Smad3 -null mice was able to reduce Mstn expression back to levels comparable to WT mice. [score:5]
The miR-27a promoter (miR-27a pro), miR-27b promoter (miR-27b pro) and the mutant miR-27b promoter reporter construct (miR-27b pro-mut) used in this study were kindly gifted by Dr Xiao Yang (State Key Laboratory of Proteomics, Genetic Laboratory of Development and Diseases, Institute of Biotechnology, Beijing, China) and have been described previously [31], [32]. [score:4]
Given that miR-27a and miR-27b have the same “seed” sequence, UGACACU, which recognizes complementary sequences in the 3′UTRs of target genes, it is not surprising that we found no difference in the ability of miR-27a or miR-27b to regulate Mstn. [score:4]
Recently published evidence suggests that miR-27 may play a role in regulating skeletal muscle fiber type-specific expression of Mstn [23]. [score:4]
Evidence suggests that miR-27a and miR-27b play an important role in controlling tissue-specific and muscle fiber type-specific expression of Mstn and regulating Mstn function during myogenesis. [score:4]
Importantly, in our current experiments we did not observe any significant difference in the ability of miR-27a or miR-27b to regulate Mstn expression or activity. [score:4]
Importantly, the elevated Mstn expression was associated with a significant decrease in both mature miR-27a and miR-27b expression in all muscle tissues isolated from Smad3 -null mice, as compared to WT mice (Figure 5B & 5C). [score:4]
AntagomiR -mediated blockade of miR-27a and miR-27b not only up regulated Mstn expression but also significantly reduced C2C12 myoblast proliferation. [score:4]
In summary, we provide further evidence to support a role for miR-27 in regulating Mstn expression. [score:4]
A role for miR-27 in regulating myogenic differentiation is not novel, in fact Crist et al recently demonstrated that miR-27b is able to negatively regulate Pax3 protein levels in adult muscle satellite cells to allow for timely entry into the myogenic differentiation program [40]. [score:3]
qPCR analysis of (F) Mstn and (G) miR-27b expression in C2C12 myoblast cultures differentiated across a time course (24 h, 48 h, 72 h and 96 h differentiation). [score:3]
However, we now show that over expression of miR-27 in vivo leads to increased numbers of Pax7 [+] cells. [score:3]
Synthetic miR-27b mimic and non -targeting miRNA negative control mimic were obtained from Dharmacon. [score:3]
However in contrast, we observed a gradual increase in miR-27b expression from 24 h through to 96 h differentiation (Figure 1G). [score:3]
Importantly, TargetScan analysis revealed an 8 mer seed match, defined as a perfect match to positions 2–8 of the mature miRNA followed by an adenine, between the miR-27a and miR-27b seed sequence and the miR-27a/b binding site in the 3′UTR of the murine Mstn gene (Figure 1A). [score:3]
Specifically, work from Allen and Loh revealed that miR-27a and miR-27b fast-twitch and slow-twitch muscle-specific expression was complementary to that of Mstn. [score:3]
qPCR analysis of (A) Mstn, (B) miR-27a and (C) miR-27b expression in M. Tibialis anterior muscle (TA), M. Gastrocnemius muscle (GAS) and M. Quadriceps muscle (QUAD) isolated from WT and Smad3 -null mice. [score:3]
Inhibition of miR-27a and miR-27b results in increased Mstn activity. [score:3]
To assess for the expression of mature miR-27a and miR-27b, cDNA was synthesized from extracted RNA using the miScript II RT kit (Cat# 218161; Qiagen), as per the manufacturer's instructions. [score:3]
Recent work from Crist et al has shown that miR-27 is able to down regulate Pax3 protein levels, without affecting the levels of Pax7 [40]. [score:2]
Nevertheless, we did note a significant reduction in the numbers of Pax7 [+] cells and activated myoblasts (MyoD [+]) upon AntagomiR -mediated blockade of miR-27a in vivo, further confirming that miR-27 is able to regulate Mstn. [score:2]
To confirm whether Smad3 is involved in Mstn regulation of miR-27a/b, C2C12 myoblasts were transfected with either the miR-27a promoter (miR-27a pro), miR-27b promoter (miR-27b pro) or a mutant miR-27b promoter reporter construct, where the smad binding site has been mutated (miR-27b pro-mut) and subjected to treatment with CMM. [score:2]
After an overnight attachment period, myoblasts were transfected with 25 nM each of AntagomiRs specific for miR-27a (AntagomiR-27a), miR-27b (AntagomiR-27b) or negative control AntagomiR (AntagomiR Neg) (Dharmacon Inc, USA) using Lipofectamine 2000 (LF2000; Invitrogen, USA), as per the manufacturer's gui delines. [score:1]
A final concentration of 50 nM each of miR-27b mimic and miRNA negative control were transfected into wild type (WT) and Smad3 -null mouse primary myoblasts using LF2000 (Invitrogen) as per the manufacturer's protocol. [score:1]
As shown in Figure 6C, addition of SIS3 was able to partially rescue the increased miR-27a- and miR-27b-promoter-reporter luciferase activity observed following treatment with CMM alone (Figure 6C). [score:1]
Treatment with CMM resulted in a significant increase in promoter-reporter luciferase activity in myoblasts transfected with either the miR-27a or miR-27b promoter constructs (Figure 6C); however, no significant increase in luciferase activity was observed in C2C12 myoblasts transfected with the mutated miR-27b promoter construct following CMM treatment (Figure 6C). [score:1]
To assess for miR-27a and miR-27b promoter reporter activity, miR-27a pro, miR-27b pro and miR-27b pro-mut constructs were electroporated (GenePulsar MXcell, Bio-rad, Hercules, CA, USA) into 1 million C2C12 cells and grown to confluency. [score:1]
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[+] score: 139
It is probable that the miR-27b -mediated down-regulation of SDF-1α in the early postburn stage delayed the wound repair, and the inhibition of miR-27b may upregulate SDF-1α protein expression and ultimately promotes MSC directional migration and wound healing. [score:12]
As expected, miR-27a- and miR-27b -mediated suppression of the Firefly/Renilla luciferase activity was abolished when we mutated the miR-27a and miR-27b binding sites in the SDF-1α-3′UTR (Figure 5D, E), suggesting that miR-27a and miR-27b inhibit SDF-1α translation by directly binding to the SDF-1α 3′UTR. [score:8]
These results show that miR-27b functionally down-regulated SDF-1α expression and eventually inhibited the migration of mMSCs to burn wound niches. [score:8]
In conclusion, our results have demonstrated that miR-27b suppressed MSC directional migration by down -regulating SDF-1α expression. [score:7]
miR-27b may be a unique signature of the stem cell niche in burned mouse skin and can suppress the directional migration of mMSCs by targeting SDF-1α by binding directly to its 3′UTR. [score:7]
We also found that several miRNAs suppressed SDF-1α protein expression, while just miR-27a and miR-27b directly bound to the SDF-1α 3′UTR. [score:6]
However, miRNA-27b could inhibit the VEGF mRNA, which suggested that miRNA-27b might inhibit the angiogenesis of the burn area (Figure S2). [score:5]
The error bars represent S. D. The above results clearly demonstrate that miR-27a and miR-27b greatly suppressed the expression of SDF-1α. [score:5]
We therefore showed that forced overexpression of miR-27b on burn wound margins significantly inhibited the mobilization of MSCs to the epidermis (Figure 7) and wound closure (Figure 8), while miR-1 and miR-27a had no obvious effects on the homing of MSCs in vivo. [score:5]
miR-27b Inhibits mMSC Directional Migration and Wound Healing Ability. [score:4]
Moreover, the forced over -expression of miR-27a and miR-27b significantly reduced the directional migration of mMSCs in vitro. [score:4]
Thus, we performed mutation assays of the putative binding sites to confirm that the SDF-1α 3′UTR is a direct target of miR-27a and miR-27b (Figure 5 E). [score:4]
First, we overexpressed specific miRNAs in mMSCs to reduce SDF-1α secretion and found that miR-1 (see Figure 6 and Figure S1), miR-27a and miR-27b significantly inhibited the migration of other normal mMSCs compared to negative controls in vitro (p<0.05) (Figure 6). [score:4]
Altogether, these results further indicate the importance of the miRNA-27b-SDF-1α -mediated inhibition of MSCs migration in the wound repair. [score:3]
However, only miR-27b in burn wound margins significantly inhibited the mobilization of MSCs to the epidermis. [score:3]
We speculated that miR-27a and miR-27b may function as chemotaxis inhibitors in burn wound healing. [score:3]
miR-27b was downregulated significantly in burned murine skin compared to the bordering normal skin. [score:3]
At the post-transcriptional level, miR-27b serves as a biological rheostat [39] whose function depends on the mutual/reciprocal actions of the ligand SDF-1α and its receptor CXCR4 expressed by stem cells and stromal cells under different alarm situations. [score:3]
The Correlation of miR-27b and SDF-1α expression was analyzed by Pearson analysis Correlation. [score:3]
The error bars represent S. D. The LV-mmu-mir-27b treatment inhibited the mobilization of mMSCs to the epidermis. [score:3]
miR-23a, miR-27a and miR-27b expression was significantly lower in the burned skin than in the normal skin (p<0.05). [score:3]
0068972.g007 Figure 7 The LV-mmu-mir-27b treatment inhibited the mobilization of mMSCs to the epidermis. [score:3]
The expression of miR-27b and SDF-1α was examined in burned murine skin tissue using quantitative real-time PCR (qPCR) and immunohistochemistry (IHC), enzyme-linked immunosorbent assay (ELISA). [score:2]
In particular, miR-27b suppressed SDF-1α protein in mMSCs most significantly compared to the control group (Figure 5A). [score:2]
The gene-specific primer pairs used to amplify specific target genes were as follows, and GenBank accession numbers also be included: mmu-miR-1(NR_029528.1): GSP, 5′-GGGGTGGAATGTAAAGAAGT-3′ and reverse, 5′-CAGTGCGTGTCGTGGAGT-3′; mmu-miR-136(AJ 459747.1): GSP, 5′-GGAACTCCATTTGTTTTGA-3′ and reverse, 5′-CAGTGCGTGTCGTGGAGT-3′; mmu-miR-214(NR_029796.1): GSP, 5′-GACAGCAGGCACAGACA-3′ and reverse, 5′-TGCGTGTCGTGGAGTC-3′; mmu-miR-23a (NR_029740.1): GSP, 5′-CCATCACATGCCAGG-3′ and reverse, 5′-CAGTGCGTGTCGTGGAGT-3′; mmu-miR-27a (NR_029746.1): GSP, 5′-GGGGTTCACAGTGGCTAA-3′ and reverse, 5′-CAGTGCGTGTCGTGGAGT-3′; mmu-miR-27b(NR_029531.1): GSP, 5′-GGGGTTCACAGTGGCTAAG′ -3′ and reverse, 5′-CAGTGCGTGTCGTGGAGT-3′; U6(NM_001204274.1): forward, 5′-GCTTCGGCAGCACATATACTAAAAT-3′ and reverse, 5′-CGCTTCACGAATTTGCGTGTCAT-3′; VEGF (NC_000083.6): forward, 5′-GTCCAACTTCTGGGCTCTTCT-3′ and reverse, 5′-CCTTCTCTTCCCCTCTCT-3′. [score:2]
The error bars represent S. D. (D) The predicted miR-27a and miR-27b binding sites in SDF-1α were mutated by site-directed mutagenesis of the miRNA seed region. [score:2]
Western blot analysis demonstrated that miR-27b caused a significant reduction of SDF-1α (p<0.05), while other miRNAs had minor or no effects on SDF-1α translation (Figure 5A), which did not confirm the results of the luciferase reporter assay. [score:2]
These results suggest that miR-23a, miR-27a, and miR-27b might be involved in the regulation of SDF-1α in the context of burned skin. [score:2]
These results demonstrate the importance of the interaction between miR-27b and SDF-1α in regulating the migration of mMSCs in wound healing. [score:2]
The expression of miR-23a, miR-27a and miR-27b were significantly lower in the burned skin compared to the normal skin (p<0.05) (Figure 4B). [score:2]
Therefore, we performed luciferase reporter assays to determine whether miR-27a and miR-27b are capable of binding the 3′UTR of SDF-1α to prevent its translation. [score:2]
To further confirm the effect of miRNA-27b on the migration and recruitment of MSCs but not the other aspects of cell behaviors, we tested the proliferation, angiogenesis and the differentiation of the MSCs. [score:1]
The concentration of IL-8 and Pan-CK were measured in the MSCs over -expressing cel-miR-67 and miR-27b using ELISA (RayBiotech, USA). [score:1]
0068972.g006 Figure 6 (A) The migration capacity of MSCs over -expressing miR-27a and miR-27b was analyzed with a transwell migration assay compared to the blank control and negative control. [score:1]
The effects of miR-27a and miR-27b on MSC migration. [score:1]
The results showed that miRNA-27b did not affect MSCs proliferation, the ability of secretion of IL-8 which is able to induce angiogenesis and cell movement, differentiation of MSCs through testing Pan-CK. [score:1]
Then, 0.1 ml LV-mmu-mir-27b (5×10 [8] TU/ml) was added to the burn wound margins in each of two separate multi-point injections. [score:1]
As shown in Figure 5A, miR-27b, miR-27a, miR-1, miR-136, and miR-214 reduced the level of SDF-1α protein. [score:1]
Beyond the findings that miRNAs may be unique signatures of different stem cell niches, our findings also suggest that antagonistic action may exist within the 3′UTR [36], possibly as a result of conformational changes occurring upon miR-27b binding. [score:1]
The error bars represent S. D. (A) The migration capacity of MSCs over -expressing miR-27a and miR-27b was analyzed with a transwell migration assay compared to the blank control and negative control. [score:1]
Lane 1, MSCs; lane 2, MSCs/cel-miR-67; lane 3, MSCs/miR-27b; lane 4, MSCs/miR-27a; lane 5, MSCs/miR-1; lane 6, MSCs/miR-23a; lane 7, MSCs/miR-136; lane 8, MSCs/miR-214. [score:1]
They were named LV-mmu-mir-1, LV-mmu-mir-136, LV-mmu-mir-214, LV-mmu-mir-23a, LV-mmu-mir-27a, LV-mmu-mir-27b, and LV-cel-mir-67 (the negative control). [score:1]
Y-chromosome and Pan-CK double -positive epidermal cells and hair follicle cells at the wound margins were decreased in the LV-mmu-mir-27b group (Figure 7). [score:1]
Figure S2 The effects of miR-27b on MSCs behavior. [score:1]
The error bars represent S. D. The correlation between mir-27b and SDF-1α were tested by Pearson analysis. [score:1]
Meanwhile, miR-27b was found negative related to the change of SDF-1α, (P<0.05) in Pearson test by Prism 5.0 (GraphPad) (Figure 4 C). [score:1]
[1 to 20 of 46 sentences]
4
[+] score: 135
Taken together, these findings suggest that hypoxia could induce c-Myc expression to inhibit the transcription of miR-23b and miR-27b in neurons, resulting in the upregulation of Apaf-1. C57BL/6 mice were employed in the present study. [score:8]
Our previous study showed that miR-23b and miR-27b in neurons, both of which are encoded by the miR-23b-27b-24–1 cluster, are downregulated during hypoxia, resulting in the upregulation of Apaf-1 and the promotion of apoptosis both in vitro and in vivo [10]. [score:7]
We found that c-Myc could directly downregulate the expression of miR-23b and miR-27b at the transcriptional level in mouse neurons. [score:7]
To further determine whether c-Myc could inhibit miR-23b and miR-27b expression in neurons, we placed a c-Myc expression vector into the neurons to elevate the c-Myc protein level (Fig. 3A). [score:7]
The acute brain injury induced by hypoxia appears to promote the expression of c-Myc and suppress the expression of miR-23b and miR-27b, consequently leading to greater neuronal apoptosis. [score:7]
Because we demonstrated that c-Myc suppressed the expression of miR-23b and miR-27b, we next tested whether c-Myc could directly bind to the promoter region of miR-23b-27b cluster. [score:6]
c-Myc downregulates miR-23b and miR-27b expression in cultured neurons at the transcriptional level. [score:6]
Furthermore, forced knockdown of c-Myc by siRNA could increase the transcription of miR-23b and miR-27b in neurons, whereas a c-Myc overexpression plasmid could inhibit the transcription of miR-23b and miR-27b in neurons. [score:6]
To further determine whether the recovered miR-23b and miR-27b expression could regulate the targeting protein Apaf-1, we assessed the protein level of Apaf-1 in neurons treated with c-Myc siRNA and subjected to anaerobic treatment (24 h). [score:6]
The elevated c-Myc level suppressed the expression of miR-23b and miR-27b, and resulted in higher Apaf-1 levels and enhanced sensitivity to apoptosis. [score:5]
Consistent with Gao’s result [24], we found that c-Myc suppressed miR-23b and miR-27b expression, and we identified two binding sites in the miR-23b-27b cluster in primary cultured neurons. [score:5]
In the present study, we observed that the expression levels of the primary transcripts of miR-23b and miR-27b were also significantly lower in the hypoxia group, suggesting that miR-23b and miR-27b may be regulated by transcription factors. [score:4]
Cortical neurons were transfected with the c-Myc siRNA; 48 h later, the neurons received anaerobic treatment (6 h), and we found that knocking down c-Myc expression restored the miR-23b and miR-27b levels (Fig. 5A-B). [score:4]
c-Myc downregulates miR-23b and miR-27b at the transcriptional level. [score:4]
Together, these findings demonstrate that c-Myc negatively regulates the expression of miR-23b and miR-27b in primary cortical neurons. [score:4]
In conclusion, these results indicate that knockdown of c-Myc alleviates neuronal apoptosis by enhancing miR-23b and miR-27b and inhibiting Apaf-1 in hypoxia -induced pathological conditions. [score:4]
We have reported that mature miR-23b and miR-27b are downregulated during hypoxia [10]. [score:4]
Previous studies have shown that c-Myc differentially regulates miR-23 and miR-27 expression at the transcriptional level in different cell types [24, 25]. [score:4]
A and B, Quantitative RT-PCR detection of the expression of mature and primary form of miR-23b and miR-27b in the cerebral cortices (A) and in primary cultures of cortical neurons (B) under conditions of normoxia or hypoxia for 6 h (n = 4, unpaired t-test, * P < 0.05, ** P < 0.01, *** P<0.001). [score:3]
D, Quantitative RT-PCR detection of the expression of mature and primary form of miR-23b and miR-27b in primary cortical neurons pre -transfected with siRNA (n = 4, unpaired t-test, * P < 0.05). [score:3]
Whether c-Myc promotes or suppresses miR-23b and miR-27b at the transcriptional level in mouse neurons remains unknown. [score:3]
We found that the expression of mature and primary form of miR-23b and miR-27b were significantly increased above control levels (Fig. 3D). [score:3]
B, Quantitative RT-PCR detection of the expression of mature and primary form of miR-23b and miR-27b in primary cortical neurons pre -transfected with siRNA under conditions of normoxia or hypoxia for 6 h (n = 5, one-way ANOVA with Newman-Keuls multiple comparison test, ns, not significant, *** P<0.001). [score:3]
c-Myc acts at an E-Box to repress miR-23b and miR-27b expression. [score:3]
Real-time PCR analysis showed that mature the expression of mature and primary form of miR-23b and miR-27b were significantly decreased (Fig. 3B). [score:3]
B, Quantitative RT-PCR detection of the expression of mature and primary form of miR-23b and miR-27b in primary cortical neurons pre -transfected with plasmids (n = 4, unpaired t-test, ** P < 0.01, and *** P<0.001). [score:3]
0120217.g001 Fig 1 A and B, Quantitative RT-PCR detection of the expression of mature and primary form of miR-23b and miR-27b in the cerebral cortices (A) and in primary cultures of cortical neurons (B) under conditions of normoxia or hypoxia for 6 h (n = 4, unpaired t-test, * P < 0.05, ** P < 0.01, *** P<0.001). [score:3]
We therefore examined the possible role of c-Myc in regulating miR-23b and miR-27b in our mo del. [score:2]
However, the mechanism by which miR-23b and miR-27b are downregulated by hypoxia has not been investigated. [score:2]
Knockdown of c-Myc recovers the miR-23b and miR-27b levels decreased by hypoxia. [score:2]
Hypoxia treatments decrease the levels of mature miR-23b and miR-27b and their primary transcripts. [score:1]
The probes for pri-miRNAs were made to order and the ID number for pri-miR-23b is Mm03306184_pri and for pri-miR-27b is Mm03306468_pri. [score:1]
We found that c-Myc could repress miR-23b and miR-27b at the transcriptional level in primary cortical neurons. [score:1]
The ID number for mature miR-23b is 000400 and for mature miR-27b is 000409. [score:1]
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5
[+] score: 128
After, 20 miRNAs were significantly upregulated more than two-fold and six miRNAs were significantly downregulated more than two-fold; miR-27b-3p was one of the most downregulated miRNAs after in HESCs from patients with endometriosis. [score:10]
Overexpression of miR-27b promotes hypertrophic cardiomyocyte growth, while its suppression leads to inhibition of hypertrophic cell growth [39]. [score:7]
In addition, Rg3 downregulated miR-27b-3p expression in HESCs. [score:6]
Transfection of the miR-27b-3p inhibitor downregulated markers of fibrosis in HESCs (Fig.   5). [score:6]
The miR-27b-3p expression was significantly downregulated in endometriosis patient’s HESCs after. [score:6]
In this study, we show that miR-27b-3p expression is elevated in the eutopic endometrium of patients with endometriosis, and Rg3E effectively reduces expression of this miRNA in HESCs from patients with endometriosis. [score:5]
Expression of miR-27b-3p was 100- to 200-fold lower after treatment with the hsa-miR-27b-3p inhibitor than that observed after treatment with the hsa-miR -negative control (Supplementary data). [score:5]
Cells were cultured to 70–80% confluence after being seeded onto 6-well plates and were transfected with hsa-mir-27b-3p inhibitor, a chemically synthesized double-stranded RNA that inhibits mature endogenous miRNA, or hsa-mir -negative as a control (Ambion by Life Technologies) with the use of Lipofectamine 2000 (Invitrogen) per the manufacturer’s instructions, at a final concentration of 50 nmol/L. [score:5]
In pulmonary fibrosis, overexpression of miR-27b increased the expression of alpha smooth muscle actin (α-SMA) [41]. [score:5]
Figure 5mRNA concentrations and protein expressions of Col-1, CTGF, Fibronectin, TGF- β1, MMP2 and MMP9 in HESCs from the patients with endometriosis after mir-27b-3p inhibitor transfection. [score:5]
Cells were transfected with miR-27b-3p inhibitor for 48 h, and then subjected to qRT-PCR and western blot analysis to determine the mRNA concentrations and protein expression levels of Col-1, CTGF, Fibronectin, TGF- β1, MMP2 and MMP9. [score:5]
Col-1 mRNA concentration and protein expression significantly decreased after treatment with the miR-27b-3p inhibitor (0.40 fold decrease, P = 0.035), whereas that of CTGF (1.02 fold increase, P = 0.979), fibronectin (0.45 fold decrease, P = 0.063), and TGF- β1 (0.45 fold decrease, P = 0.057) did not significantly change. [score:5]
In the eutopic endometrium of patients with endometriosis, miR-27b-3p expression was approximately two-fold higher than that observed in patients without the disease (fold change 0.28 vs. [score:5]
The transfection experiment was specifically proceeded with miR-27b-3p inhibitor that other fibrosis markers which were not significantly changed may be regulated mainly by other types of miRNAs. [score:4]
Among the endometriosis-affected miRNAs, miR-27b-3p was especially related to the development of fibrosis and inhibition of miR-27b significantly reduced fibrosis. [score:4]
To validate the miRNA microarray results, expression levels of miR-27b-3p were compared between eutopic endometria from patients with endometriosis and those without the disease. [score:4]
More importantly, decreased miR-27b by demonstrates that Rg3 may be effective for reducing the fibrotic nature of the disease. [score:3]
All these studies have shown that miR-27b expression is induced by TGF- β1, which is also related to fibrosis. [score:3]
After, miR-27b-3p expression significantly decreased in HESCs (0.51 fold decrease, P = 0.029) (Fig.   4(b), Table  2); however, similar changes were not observed in Ishikawa cells. [score:3]
miR-27b-3p Inhibitor Transfection and Western Blot. [score:3]
miR-27b expression significantly increased in both the sclerotic intima and serum samples of arteriosclerosis obliterans patients [40]. [score:3]
Figure 3Expressions of miR-27b-3p in eutopic endometrium of the patients with and without endometriosis. [score:3]
MiR-27b-3p is known for its correlation with fibrosis and its downregulation by Rg3E demonstrates the possibility of Rg3E decreasing fibrotic nature of endometriosis. [score:3]
MMP2 and MMP9, markers of invasion, were also affected by transfection of the miR-27b-3p inhibitor. [score:3]
Among the miRNAs examined in this study, miR-27b was particularly highly expressed in the endometrium of patients with endometriosis. [score:3]
Figure 4Expressions of miR-27b-3p in (a) Ishikawa cell lines and (b) HESCs from the patients with endometriosis after. [score:3]
Several previous studies suggest that miR-27b is involved in fibrosis development. [score:2]
The basal miR-27b-3p expression was significantly increased in endometriosis patients compared to control. [score:2]
We showed that Rg3E and miR-27b-3p inhibition effectively reduce endometriosis fibrotic potential using a contraction gel assay and an in vivo mouse mo del. [score:2]
The treatment mechanism involved changes in several miRNAs, including miR-27b-3p. [score:1]
Quantitative real-time PCR for miRNAs was performed using a Taqman [®] Universal Master Mix II, no UNG (Applied Biosystems, Foster City, CA, USA) with sets for miR-27b-3p and U6 snRNA (Applied Biosystems, Foster City, CA, USA). [score:1]
miRNA Profiling after Rg3E Treatment and Validation of miR-27b-3p in Endometriosis. [score:1]
Therefore, increased expression of miR-27b in endometriosis may be related to its fibrotic characteristics. [score:1]
To evaluate transfection efficacy, miR-27b-3p expression was measured 48 h after transfection with an hsa-miR -negative control and hsa-miR-27b-3p inhibitor in HESCs from the endometrium of the patients with endometriosis. [score:1]
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6
[+] score: 88
b miRNA RT-qPCR analysis showing the complete regulation of Hsa-miR-93, Hsa-miR-20a, Hsa-miR-125b and Hsa-miR-27b and, significant increase in the expression of Hsa-miR-1260 and Hsa-miR-1224-3p in metastatic tumors as compared to the non-metastatic xenograftTo validate the altered expression levels observed with whole genome miRNA array, we examined the expression levels of select miRNAs including hsa-miR-1260, hsa-miR-1224-3p (showing significant upregulation; see Fig.   2), hsa-miR-93, hsa-miR-20a, hsa-miR-125b, hsa-miR-27b (showing significant downregulation; see Fig.   3a), using individual miRNA QPCR analysis. [score:13]
b miRNA RT-qPCR analysis showing the complete regulation of Hsa-miR-93, Hsa-miR-20a, Hsa-miR-125b and Hsa-miR-27b and, significant increase in the expression of Hsa-miR-1260 and Hsa-miR-1224-3p in metastatic tumors as compared to the non-metastatic xenograft To validate the altered expression levels observed with whole genome miRNA array, we examined the expression levels of select miRNAs including hsa-miR-1260, hsa-miR-1224-3p (showing significant upregulation; see Fig.   2), hsa-miR-93, hsa-miR-20a, hsa-miR-125b, hsa-miR-27b (showing significant downregulation; see Fig.   3a), using individual miRNA QPCR analysis. [score:13]
To define the effect of characterized metastamiRs on the putative target proteins, we adopted two approaches: (i) inhibited hsa-miR-1224-3p or hsa-miR-1260 (both significantly upregulated) and (ii) functionally mimicked hsa-miR-125b, hsa-miR-27b, hsa-miR-93 or hsa-miR-20a (all significantly downregulated) and examined for the miRNA -dependent modulations in protein targets. [score:11]
In order to validate the miRNA expression obtained from whole genome profiling, expression of selected metastamiRs, including hsa-miR-1224-3p, hsa-miR-1260 (both significantly upregulated), hsa-miR-125b, hsa-miR-27b, hsa-miR-93,and hsa-miR-20a (all significantly downregulated) were confirmed using QPCR. [score:11]
First, MSDACs transiently transfected with mimics for hsa-miR-125b, hsa-miR-27b, hsa-miR-93 or hsa-miR-20a (those exhibited complete suppression in aggressive disease) and examined for the regulation of their corresponding target proteins (Fig.   6a). [score:8]
Thus, we validated our microarray results with RT-qPCR for upregulation (Hsa-miR-1260; Hsa-miR-1224-3p) and downregulation (Hsa-miR-20a, Hsa-miR-27b, Hsa-miR-125b, Hsa-miR-93) profiles (see Fig.   3b). [score:7]
miRNA mimic (hsa-miR-125b, hsa-miR-27b, hsa-miR-93, hsa-miR-20a) and inhibitor (hsa-miR-1224-3p, hsa-miR-1260) approach for select miRNAs revealed the direct influence of the altered metastamiRs in the regulation of identified protein targets. [score:7]
Transient transfection of MSDACs with hsa-miR-125b-, hsa-miR-27b-, hsa-miR-93- or hsa-miR-20a- mimics (MISSION® microRNA Mimics, Sigma-Aldrich) as well as hsa-miR-1224-3p- and hsa-miR-1260 -inhibitors (MISSION® Synthetic miRNA Inhibitors, Sigma-Aldrich) were carried out by using either TurboFectin 8.0 reagent (Origene) or Neon electroporation transfection system (Life Technologies). [score:5]
Interestingly, mimicking hsa-miR-27b did not inhibit the expression of EGFR and VEGF in MSDACs. [score:5]
b Histograms of mean cell–Alexa Fluor intensity obtained from Columbus automated batch analysis showing alterations in the expression (i) GRB10, MMP2, p38, STAT3, TNFα and VEGF in cells with hsa-miR-125b mimic, (ii) EGFR FOSB, kRAS, p38, PTPN3 and VEGF in hsa-miR-27b mimic transfected cells, (iii) ASK1, CREB, MMP2, MMP3/10, PTPN3, STAT3and VEGF in MSDACs with hsa-miR-20a mimic and, (iv) MMP2, MMP3/10, PTPN3 and STAT3 with hsa-miR-93 mimic in MSDACs. [score:3]
Similarly, functionally mimicking hsa-miR-27b resulted in the profound (P < 0.001) inhibition of FOSB, kRAS, p38 and PTPN3 (Fig.  6b i i). [score:3]
Compared to the non-metastatic xenograft, we observed a complete (P < 0.001) decrease in the expression of hsa-miR-93, hsa-miR-20a, hsa-miR-125b, and hsa-miR-27b (Fig.   3b). [score:2]
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7
[+] score: 77
Other miRNAs from this paper: mmu-mir-27a
86±8.33 * Inhibitor-neg 180.26±24.82 0.82±0.13 194.89±24.20 88.91±8.96 miR-27a inhibitor230.25±26.17 *1.42±0.16 *241.70±37.79 *128.15±16.58 * miR-27b inhibitor228.91±25.73 *1.38±0.10 *232.03±38.21 *124.57±17.94 * miR-27a inhibitor+LPL-siRNA163.73±16.25 [#]0.85±0.18 [#]187.52±28.83 [#]78. [score:9]
0157085.g008 Fig 8 MiR-27, binding to the LPL 3’UTR to accelerate degradation or repress post-transcriptional expression of mRNA, can inhibit the expression of LPL, and then attenuate lipid accumulation and secretion of proinflammatory cytokines. [score:6]
In our study, as shown in Fig 8, miR-27 is negatively associated with the expression and activity of LPL through directly targeting the 3’UTR of macrophage LPL, and serves as an important modulator contributing to the macrophage cellular lipid homeostasis and inflammatory response related to atherogenesis. [score:6]
MiR-27, binding to the LPL 3’UTR to accelerate degradation or repress post-transcriptional expression of mRNA, can inhibit the expression of LPL, and then attenuate lipid accumulation and secretion of proinflammatory cytokines. [score:6]
Recent evidence indicates that miR-27b is a strong regulator of lipid metabolism in the human liver via regulating the expression of several of key lipid metabolism-related genes, including ABCA1, LDLR, Angptl3 and Gpam[27, 41]. [score:5]
It may be speculated that a novel specific method that effectively regulates miR-27 expression within macrophages might be used to control the development of atherosclerosis. [score:5]
We showed that miR-27 attenuated lipid accumulation and secretion of the pro-inflammatory cytokines, leading to a reduction in the development of atherosclerotic lesions in apoE KO mice, at least partially, by repressing the expression of LPL directly. [score:5]
A role for miR-27 in negative regulation of lipid accumulation and proinflammatory cytokine secretion through targeting LPL gene. [score:4]
To date, however, it is still not clear whether miR-27 plays a role in the development of atherosclerosis through targeting macrophage LPL in vivo. [score:4]
These anti-atherosclerotic effects of miR-27a/b may result from miR-27 -mediated regulation of the expression of LPL, suggesting a role for scavenger receptors in lipid uptake. [score:4]
In addition, the expression levels of miR-27 are closely associated with clinical factors and the prognosis of patients with atherosclerosis obliterans, suggesting that it might serve as a potential biomarker for atherosclerosis[20, 42]. [score:3]
#P<0.05 vs miR-27b inhibitor. [score:3]
To fully understand the connection between the miR-27 and atherosclerosis, more studies are required to explore further the potential mechanisms underlying miR-27 effects on lipid metabolism and pro-inflammatory pathways through targeting the LPL gene in vivo. [score:3]
MiR-27 was found to inhibit adipocyte differentiation that is closely associated with the onset of obesity[25, 26], and also participate in lipid metabolism in the liver[27]. [score:2]
At the same time, our results have shown a positive effect of miR-27 on the pathological process of atherosclerosis through reducing accumulation of intracellular lipids and secretion of pro-inflammatory cytokines in apoE KO mice. [score:1]
AG-NC: miR-27a/b agomir negative control; AGa: miR-27a agomir; AGb: miR-27b agomir; AN-NC: miR-27a/b antagomir negative control; ANa: miR-27a antagomir; ANb: miR-27b antagomir; TC: total cholesterol; FC: free cholesterol; CE: cholesterol ester. [score:1]
AG-NC: miR-27a/b agomir negative control; AGa: miR-27a agomir; AGb: miR-27b agomir; AN-NC: miR-27a/b antagomir negative control; ANa: miR-27a antagomir; ANb: miR-27b antagomir; IL-1β: Interleukin-1β IL-6: Interleukin-6; MCP-1: monocyte chemotactic factor-1; TNF-α: tumor necrosis factor alpha. [score:1]
Furthermore, it has been reported that miR-27 has provided a potent atheroprotective function in endothelial cells activated by laminar shear stress[43]. [score:1]
Recently, a notable role for miR-27 in the pathogenesis of atherosclerosis has been noticed and studied extensively, although previous studies about miR-27 were more involved in the field of tumor research. [score:1]
The magic and mystery of microRNA-27 in atherosclerosis. [score:1]
AG-NC: miR-27a/b agomir negative control; AGa: miR-27a agomir; AGb: miR-27b agomir; AN-NC: miR-27a/b antagomir negative control; ANa: miR-27a antagomir; ANb: miR-27b antagomir; BW: body weight; TG: triglyceride; TC: total cholesterol; HDL-C: high density lipoprotein cholesterol; LDL-C: low-density lipoprotein cholesterol. [score:1]
These findings suggest that miR-27 may have a close relationship with atherosclerosis. [score:1]
It has been proposed that two isoforms of the miR-27 family, miR-27a and -27b present in the macrophage cell lines, may participate in the initiation and progression of atherosclerosis as we recently reviewed[20]. [score:1]
ApoE KO mice fed high-fat diet were given a tail vein injection with miR-27 agomir/antagomir or their respective scrambled controls to explore the potential effects of miR-27. [score:1]
79±11.84 [#] miR-27b inhibitor+LPL-siRNA159.86±12.13 [#]0.80±0.14 [#]185.46±28.64 [#]77.57±13.04 [#] LPL235.49±15.59 *1.76±0.15 *250.95±22.15 *140.75±21.22 * LPL-siRNA73.79±12.93 *0.45±0.13 *104.84±19.66 *49.67±12.77 * The concentrations of inflammatory cytokines secreted in 24 h culture supernatants by stimulating THP-1 macrophages with various factors were measured by ELISA. [score:1]
Many pieces of research have shown that miR-27 is involved in angiogenesis, adipogenesis, oxidative stress, insulin resistance, which are the known processes associated with atherosclerosis. [score:1]
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8
[+] score: 69
Interestingly, Wnt5a can up-regulate miR-27b which miRNA has been reported to bind to the highly conserved binding site in the 3′UTR of PPARgamma [48] and suppress its expression [49]. [score:8]
Binding of miR-27b to its target sequence can suppress PPARgamma expression [49] and augment VEGF-A induced angiogenesis [50]. [score:7]
While canonical Wnts down-regulate PPARgamma directly, non-canonical Wnt5a increases miR27b that is known regulator of PPARgamma. [score:6]
Additionally, miR-27b can also block the Wnt5a target NF-kappaB [64] and the TGF-beta target, Gremlin-1 [65]. [score:5]
Wnt5a induces miR-27b a regulator of both PPARgamma expression and blood vessel branching. [score:4]
In the literature PPARgamma has been described to have a highly conserved binding site in its 3′UTR that is a direct target of miR-27b [48]. [score:4]
Remarkably, rhWnt5a could not up-regulate miR-27b in the presence of a PPARgamma agonist, only if the antagonist was present (Fig.   3e). [score:4]
d, miR-27b is up-regulated by rhWnt5a in 3D lung aggregate cultures, while neither miR-27b nor miR-200b was affected by rhWnt11. [score:4]
Importantly, both miR-27b as well as another miRNA, miR-200b can inhibit blood vessel branching during angiogenesis [51, 52]. [score:3]
One-way ANOVA, post hoc Bonferroni, n = 6. e, VEGF-A and miR-27b expression levels after 10 μM RSG (PPARgamma agonist) and 10 μM GW9662 (PPARgamma antagonist) and combination treatment with rhWnt5a. [score:3]
Karbiener M Fischer C Nowitsch S Opriessnig P Papak C Ailhaud G microRNA miR-27b impairs human adipocyte differentiation and targets PPARgammaBiochem. [score:3]
Interestingly, while rhWnt11 had no effect on either miRNAs (Fig.   3d), miR-27b expression was significantly increased by rhWnt5a treatment (Fig.   3d), while miR-200b levels were unaffected. [score:3]
Inhibitors of branching and tube formation like miR-200b [63] and miR-27b [51] are both increased in SCC compared to AC potentiating differences in the actual blood vessel formation and pattern in tumors of squamous histology. [score:2]
Macrophage pro-angiogenic miRNA, miR-27b, is under NF-kB transcription regulation. [score:2]
As only miR-27b is regulated by Wnt5a, further studies are needed to find the molecules that control miR-200b. [score:2]
As alternative signaling pathways, such as basic fibroblast growth factor (bFGF), platelet derived growth factor (PDGF) as well as miRNAs, especially the pro-angiogenic miR-27b and the miR-200 family [17, 18] also play a significant role in the regulation of angiogenesis; solely blocking VEGF-A simply cannot provide a therapeutic solution in NSCLCs [19]. [score:2]
c, miR-27b and miR-200b expression levels are significantly lower in AC compared to SCC. [score:2]
Graham JR Williams CMM Yang Z MicroRNA-27b targets gremlin 1 to modulate fibrotic responses in pulmonary cellsJ. [score:2]
Thulasingam S Massilamany C Gangaplara A Dai H Yarbaeva S Subramaniam S miR-27b*, an oxidative stress-responsive microRNA modulates nuclear factor-kB pathway in RAW 264.7 cellsMol. [score:1]
PPARgamma, VEGF-A, Wnt5a, miR-27b and miR-200b levels were determined in resected adenocarcinoma and squamous cell carcinoma samples by qRT-PCR and. [score:1]
Finally, it may be possible in the future to use serum levels of Wnt5a, miR-27b, PPARgamma levels and/or activity of the tumor tissue as prognostic markers to identify groups of patients that are at higher risk of developing hemorrhage if treated with anti-angiogenic therapies. [score:1]
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[+] score: 37
Also, mRNA levels of the tumor suppressor gene Fbxw7, a known target of miR-27 [39], was down-regulated (P<0.01) in the hearts of CR vs. [score:8]
We also validated by qPCR the expression levels of known targets of three miR (miR-27, -29 and -214), which were up-regulated in the CR group. [score:8]
0130658.g006 Fig 6 (A) qPCR validation of selected miRs from the microRNA array showing significant down-regulation of miR-21 and miR-92a and significant up-regulation of miR-27, miR-29, miR-208 and miR-214 in CR compared to Ad lib. [score:6]
We then annotated the enrichment map with the predicted targets of two miR with the highest fold change in CR (miR-27 and -29) to highlight gene sets that are significantly modulated (hyper-geometric P<0.05) as a percentage of miR targets (Fig 6B and 6C). [score:5]
In addition, miR-27, miR-29, miR-208 and miR-214 were significantly up-regulated in CR as compared to AL groups (+2.969±0.5318, P<0.05; +7.483±1.084, P<0.002; +2.483±0.9468, P<0.009; and +2.003±0.5865, P<0.02; fold change respectively, N = 3) (Fig 6A). [score:3]
Most importantly we show that both miR-27 and miR-29 have overlapping targets associated with ECM organization, angiogenesis, cell migration, cell adhesion and cytoskeletal organization. [score:3]
Both miR-27 and miR-29 showed overlapping targets in pathways associated with ECM organization, angiogenesis, cell migration, adhesion and cytoskeletal organization. [score:3]
The enrichment map was further annotated using a post analysis using mir-29 and mir-27 gene sets to highlight enriched pathways (blue or red nodes) that contain a statistically significant amount of B) miR-27 or C) mir-29 targets (as calculated using the hypergeometric distribution, p-value < 0.05). [score:1]
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10
[+] score: 32
Interestingly, analyzing together the sequencing of EVs and gene expression data of UCB-CD34+ cells treated with EVs, by Ingenuity Pathways Analysis software, we identify at least one down-regulated target gene for each EVs miRNA (e. g., miR-3168/LYZ, miR-27b-3p/ZFP36,miR21-5p/ANXA1) (Table 1). [score:8]
Finally, gene expression profile identified 103 up-regulated genes (e. g., IL6, CSF2, CCL3) that, by IPA, were found under the control of miRNA targeted genes (e. g., ZFP36/miR-27b-3p). [score:8]
To validate this correlation, we transfected five EVs miRNAs (miR-27b-3p, miR-10a-5p, miR-21-5p, miR-181a-5p and miR92a-3p) in UCB-CD34+ cells (Figure 3B) confirming the down-regulation of their predicted target genes (miR-27b-3p/MPL and ZFP36, miR-10a-5p/MPL, miR-21-5p/ANXA1, miR-181a-5p/CEBPA and EGR2, miR92a-3p/ CEBPA and EGR2) (Figure 3C). [score:6]
By contrast, over -expression of miR-27b-3p and miR-10a-5p showed a reduction of CD38 expression, i. e. a phenotypic pattern typical of undifferentiated stem cells. [score:5]
Furthermore, using IPA, we found that some of them (e. g., IL1b, CSF2, and CCL3) are under the control of genes targeted by miRNAs present in EVs (e. g., ZFP36/miR-27b-3p and miR-423-5p, ABCA1/ miR-27b-3p) (Figure 6C). [score:3]
To demonstrate that a decrease of cell differentiation is induced by BM-MSC EVs miRNAs we transfect together miR-27b-3p and miR-10a-5p (Figure 5C). [score:1]
UCB-CD34+ were transfected with 60 nM of miRNA precursor molecules (miR-27b-3p mimic, miR-10a-5p mimic, miR-21-5p mimic, miR-181a-5p mimic and miR92a-3p mimic) (Life Technologies) or negative control (Life Technologies) using Lipofectamine 2000 (Life Technologies), according to the manifacturer's instructions. [score:1]
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[+] score: 30
Other miRNAs from this paper: hsa-mir-27b
These results are in accordance with a recent report that describes that mir-27b can suppress the directional migration of MSC by downregulating SDF1α expression by binding indirectly to the SDF1α 3′UTR [44]. [score:10]
A recent report describes that mir-27b can suppress the directional migration of MSCs by downregulating SDF1 α expression by binding directly to the SDF1 α 3′UTR [44]. [score:10]
In our conditions, hMSCs might have acquired in vivo a high level CXCR4 expression and migrated in irradiated liver expressing high levels of SDF1 α. A high level of SDF1 α might be related to a low level of mir-27b. [score:5]
We conclude that hMSC engraftment is related to a low level of mir-27b. [score:1]
A high level of SDF1 α might be related to a low level of mir-27b. [score:1]
The level of mir-27b was more elevated in the liver of ungrafted mice in comparison to that of the liver containing hMSCs (P < 0.05). [score:1]
We conclude that hMSCs engraftment is related to a low level of mir-27b. [score:1]
Furthermore, the level of mir-27b is more elevated in the liver of ungrafted mice in comparison with the liver containing hMSCs. [score:1]
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[+] score: 29
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-20a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-27a, hsa-mir-92a-1, hsa-mir-92a-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-15b, mmu-mir-23b, mmu-mir-130a, mmu-mir-133a-1, mmu-mir-140, mmu-mir-24-1, hsa-mir-196a-1, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, mmu-mir-206, hsa-mir-30c-2, hsa-mir-196a-2, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-200b, mmu-mir-301a, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-15b, hsa-mir-23b, hsa-mir-27b, hsa-mir-130a, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-140, hsa-mir-206, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-196a-1, mmu-mir-196a-2, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-18a, mmu-mir-20a, mmu-mir-24-2, mmu-mir-27a, mmu-mir-92a-2, hsa-mir-200c, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-17, mmu-mir-19a, mmu-mir-200c, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-19b-1, mmu-mir-92a-1, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-301a, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, hsa-mir-196b, mmu-mir-196b, dre-mir-196a-1, dre-mir-199-1, dre-mir-199-2, dre-mir-199-3, hsa-mir-18b, dre-let-7a-1, dre-let-7a-2, dre-let-7a-3, dre-let-7a-4, dre-let-7a-5, dre-let-7a-6, dre-let-7b, dre-let-7c-1, dre-let-7c-2, dre-let-7d-1, dre-let-7d-2, dre-let-7e, dre-let-7f, dre-let-7g-1, dre-let-7g-2, dre-let-7h, dre-let-7i, dre-mir-1-2, dre-mir-1-1, dre-mir-15a-1, dre-mir-15a-2, dre-mir-15b, dre-mir-17a-1, dre-mir-17a-2, dre-mir-18a, dre-mir-18b, dre-mir-18c, dre-mir-19a, dre-mir-20a, dre-mir-23b, dre-mir-24-4, dre-mir-24-2, dre-mir-24-3, dre-mir-24-1, dre-mir-27a, dre-mir-27b, dre-mir-27c, dre-mir-27d, dre-mir-27e, dre-mir-30c, dre-mir-92a-1, dre-mir-92a-2, dre-mir-92b, dre-mir-130a, dre-mir-133a-2, dre-mir-133a-1, dre-mir-133b, dre-mir-133c, dre-mir-140, dre-mir-196a-2, dre-mir-196b, dre-mir-200a, dre-mir-200b, dre-mir-200c, dre-mir-206-1, dre-mir-206-2, dre-mir-301a, dre-let-7j, hsa-mir-92b, mmu-mir-666, mmu-mir-18b, mmu-mir-92b, mmu-mir-1b, dre-mir-196c, dre-mir-196d, mmu-mir-3074-1, mmu-mir-3074-2, hsa-mir-3074, mmu-mir-133c, mmu-let-7j, mmu-let-7k, dre-mir-24b
miRNA Embryonic age Expression profile mir15a 48 and 72 hpf Midbrain, MHB, notochord mir15b 48 and 72 hpf Midbrain, neurocranium, notochord mir23b 30, 48, and 72 hpf Somites, lens, pharyngeal arches, notochord mir27b 48 and 72 hpf mir30c 48 and 72 hpf Brain, neurocranium, eye, heart mir130a 48 and 72 hpf Brain, gut tube, heart, eye mir133b 30, 48, and 72 hpf Notochord mir301a 48 and 72 hpf Forming cartilage Midbrain, neurocranium, eye, trigeminal ganglia Figure 5 Expression of mir23b in zebrafish embryos. [score:5]
miRNA Embryonic age Expression profile mir15a 48 and 72 hpf Midbrain, MHB, notochord mir15b 48 and 72 hpf Midbrain, neurocranium, notochord mir23b 30, 48, and 72 hpf Somites, lens, pharyngeal arches, notochord mir27b 48 and 72 hpf mir30c 48 and 72 hpf Brain, neurocranium, eye, heart mir130a 48 and 72 hpf Brain, gut tube, heart, eye mir133b 30, 48, and 72 hpf Notochord mir301a 48 and 72 hpf Forming cartilage Midbrain, neurocranium, eye, trigeminal ganglia Figure 5 Expression of mir23b in zebrafish embryos. [score:5]
One of the interesting aspects our data analysis (Figure 1) is that Mir27b expression is also present in the developing midface, with its expression mirroring that of Mir23b. [score:5]
mir23b and mir27b are separated by less than 200 bp, though it is not clear that their expression is co-regulated. [score:4]
Cardiomyocyte overexpression of miR-27b induces cardiac hypertrophy and dysfunction in mice. [score:3]
MicroRNA profiling during mouse ventricular maturation: a role for miR-27 modulating Mef2c expression. [score:3]
This is especially true for Mir23b and Mir27b, as while both work concurrently to drive cardiomyocyte development from ES cells in vitro, Mir23b subsequently controls the later beating phenotype of differentiated cells while Mir27b functions to inhibit this event (Chinchilla et al., 2011; Wang et al., 2012). [score:3]
In mouse, Mir23b is part of a miRNA cluster that includes Mir23b, Mir27b, Mir3074.1, and Mir24.1. [score:1]
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[+] score: 24
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-16-1, hsa-mir-17, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-23a, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-16-2, mmu-mir-23b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-127, mmu-mir-128-1, mmu-mir-132, mmu-mir-133a-1, mmu-mir-188, mmu-mir-194-1, mmu-mir-195a, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, mmu-mir-205, mmu-mir-206, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-122, mmu-mir-30e, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-205, hsa-mir-211, hsa-mir-212, hsa-mir-214, hsa-mir-217, hsa-mir-200b, hsa-mir-23b, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-128-1, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-127, hsa-mir-138-1, hsa-mir-188, hsa-mir-194-1, hsa-mir-195, hsa-mir-206, mmu-mir-19b-2, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-23a, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-27a, mmu-mir-31, mmu-mir-351, hsa-mir-200c, mmu-mir-17, mmu-mir-19a, mmu-mir-100, mmu-mir-200c, mmu-mir-212, mmu-mir-214, mmu-mir-26a-2, mmu-mir-211, mmu-mir-29b-2, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-19b-1, mmu-mir-138-1, mmu-mir-128-2, hsa-mir-128-2, mmu-mir-217, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-379, mmu-mir-379, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-412, mmu-mir-431, hsa-mir-431, hsa-mir-451a, mmu-mir-451a, mmu-mir-467a-1, hsa-mir-412, hsa-mir-485, hsa-mir-487a, hsa-mir-491, hsa-mir-503, hsa-mir-504, mmu-mir-485, hsa-mir-487b, mmu-mir-487b, mmu-mir-503, hsa-mir-556, hsa-mir-584, mmu-mir-665, mmu-mir-669a-1, mmu-mir-674, mmu-mir-690, mmu-mir-669a-2, mmu-mir-669a-3, mmu-mir-669c, mmu-mir-696, mmu-mir-491, mmu-mir-504, hsa-mir-665, mmu-mir-467e, mmu-mir-669k, mmu-mir-669f, hsa-mir-664a, mmu-mir-1896, mmu-mir-1894, mmu-mir-1943, mmu-mir-1983, mmu-mir-1839, mmu-mir-3064, mmu-mir-3072, mmu-mir-467a-2, mmu-mir-669a-4, mmu-mir-669a-5, mmu-mir-467a-3, mmu-mir-669a-6, mmu-mir-467a-4, mmu-mir-669a-7, mmu-mir-467a-5, mmu-mir-467a-6, mmu-mir-669a-8, mmu-mir-669a-9, mmu-mir-467a-7, mmu-mir-467a-8, mmu-mir-669a-10, mmu-mir-467a-9, mmu-mir-669a-11, mmu-mir-467a-10, mmu-mir-669a-12, mmu-mir-3473a, hsa-mir-23c, hsa-mir-4436a, hsa-mir-4454, mmu-mir-3473b, hsa-mir-4681, hsa-mir-3064, hsa-mir-4436b-1, hsa-mir-4790, hsa-mir-4804, hsa-mir-548ap, mmu-mir-3473c, mmu-mir-5110, mmu-mir-3473d, mmu-mir-5128, hsa-mir-4436b-2, mmu-mir-195b, mmu-mir-133c, mmu-mir-30f, mmu-mir-3473e, hsa-mir-6825, hsa-mir-6888, mmu-mir-6967-1, mmu-mir-3473f, mmu-mir-3473g, mmu-mir-6967-2, mmu-mir-3473h
The study revealed downregulation of miR-205, miR-27, miR-31, and miR-29 in the cbs [+/–] retinas, these miRNAs were also reported to be downregulated in vitreous [68] and plasma of AMD patients [69]. [score:7]
A recent study also demonstrated that knockdown of miR-27, which downregulates the antiangiogenic factors Sprouty2 and semaphorin 6A (Sema6A), is protective against laser -induced choroidal neovascularization [70]. [score:5]
The study revealed downregulation of miR-205, miR-27, miR-31, and miR-29 in the cbs [+/–] retinas. [score:4]
Consistently with the microarray results, miR-205 (p value = 0.001), miR-206 (p value = 0.01) and miR-27 (p value = 0.04) were significantly downregulated in cbs [+/–] compared to control cbs [+/+] (p value < 0.05). [score:3]
Furthermore, the pathway analysis links a group of miRNAs that were differentially expressed in cbs [+/–] retina to oxidative stress pathway such as miR-205, miR-206, miR-217, miR-30, miR-27, miR-214 and miR-3473. [score:3]
miR-205, miR-27, miR-29 and miR-31 were significantly changed in our cbs [+/–] retina microarray and were also reported to be involved in AMD. [score:1]
Other miRNAs were linked to the hypoxia signaling pathway, for instance, miR-205, miR-214, miR-217, miR-27, miR-29, miR-30 and miR-31. [score:1]
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[+] score: 22
Of these differentially expressed miRNAs, miR-27b (downregulated in OA) directly targets MMP-13 expression (Stone et al., 2011); miR-22 (upregulated in OA) directly regulates PPARA and BMP-7 expression in cartilage; miR-9 inhibits MMP13 secretion in isolated human chondrocytes; and miR-146a is highly expressed in early OA cartilage and has been shown to control knee joint homeostasis and OA -associated algesia by balancing inflammatory responses in the cartilage and synovium. [score:22]
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[+] score: 22
First, the 3′untranslated region (3′UTR) of PPARγ contains a binding site for miR-27, and miR-27 targets PPARγ mRNA in cardiomyocytes [34] and macrophages [35]. [score:5]
Further studies will be required to fully elucidate the molecular mechanisms by which hypoxia increases miR-27 expression and if preventing increases in miR-27a levels is sufficient to prevent or reverse hypoxic -induced ET-1 expression and PH in vivo. [score:5]
The current study focused on miR-27 because it: 1) regulates PPARγ, 2) is highly expressed in the lung and heart [49]– [51], 3) is increased in the lungs of animals with PH [22] and in PASMC isolated from patients with IPAH [30], and 4) participates in the regulation of proliferation and differentiation in multiple cell types [23], [35], [45], [52]– [56]. [score:5]
However the precise mRNA targets regulated by miR-27 and their contribution to the pathogenesis of PH have not been defined. [score:4]
Second, the miR-27 gene family (miR-23a∼27a∼24-2 cluster) contributes to regulation of hypoxic responses including [36]– [38], cell cycle progression, proliferation, and hypertrophy [36]. [score:2]
Third, miR-27 is increased in the lungs of animals with PH [22] and in human pulmonary artery smooth muscle cell (HPASMC) isolated from patients with idiopathic PAH (IPAH) [30]. [score:1]
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[+] score: 19
Given that microRNAs (miRNAs) modulate pathophysiology of cardiovascular diseases through regulation of gene expression [7], [8], [9], [47], we determined whether BMPCs administration after MI regulates miRNAs (like miR-21, miR-27, miR-29, miR-155, miR-30a and miR-133a) that have been shown to play a role in fibrosis in various tissues/organs [8], [11], [12]. [score:7]
To determine whether BMPCs regulate fibrosis-related miRNAs in infarcted heart, we injected mouse BMPCs in infarcted hearts of C57BLKS/J mice and determined (at 3 days post-MI) the expression of miRNAs (miR-21, miR-27, miR-29, miR-155, miR-30a and miR-133a, which have been shown to play a role in fibrosis [9], [10], [11], [24], [25]). [score:4]
Figure 1 depicts that saline -treated MI mice showed a significant increase in expression of miR-21 and miR-155 (P<0.01; Figures 1A and 1B) and decrease in miR-29 and miR-133a (P<0.01; Figures 1C and 1D) levels with non-significant reducing trend of miR-27 and miR-30a (Figures S4. [score:3]
In contrast, the expression of miR-27 and 30a was not affected by BMPC therapy (Figure S4. [score:3]
BMPC therapy did not affect miR-27 (A) and miR-30a (B) in comparison with saline -treated group. [score:1]
Although the role miR-27 and miR-30a in fibrosis has been established in other organs systems [12], [48], their levels remained unchanged in the present study. [score:1]
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[+] score: 18
Some of the important miRs with known/putative targets and differentially regulated by TWEAK are presented in Figure 3. Our results showed that TWEAK reduced the expression of muscle-specific miR-1, miR-133a, miR-133b and miR-206 in addition to several other miRs including miR-27, miR-23, miR-93, miR-199, miR-107, and miR-192 (Figure 3A). [score:6]
Low-density miRNA array of TWEAK -treated C2C12 myotubes showed down-regulation of miR-1, miR-133a, miR-133b, miR-206, miR-27, miR-23, miR-93, miR-199, miR-107, and miR-192. [score:4]
miR-148b −2.6183 decrease apoptosis miR-152 −2.3341 Increase cell growth miR-17 −6.2545 Bcl2, N-myc miR-181c −3.5756 proliferation and remo deling of muscles miR-190b −2.2 Binds to Ubiquitin-specific protease 46, increase cell growth miR-192 −2.4871 Increase cell growth miR-199a-3p −1.9 Activin receptor IIA, Map3k4 miR-218-1 −2.2887 Increase cell growth miR-23b −2.1623 Increase Cell growth, proliferation miR-26a −2.4565 decrease proapoptotic signaling miR-27a −2.7 Ubiquitin-conjugating enzyme E2N miR-27b −3 Ubiquitin-conjugating enzyme E2N miR-296-3p −7.3378 Increase cell growth, decrease apoptosis miR-322 8.7 Hydroxysteroid (17-beta) dehydrogenase 7 miR-455 129.249 Up-regulated brown adipocyte differentiation miR-470 3.2 TGFB -induced factor homeobox 1 miR-715 18.25 Fucosyltransferase 1 miR-7a −6.2174 Increase cell growth, decrease apoptosis miR-93 −48.423 Map3k14 (NIK) miR-98 1.8 Tripartite motif-containing 6, insulin-like growth factor 2 mRNA binding protein 1 A) C2C12 myotubes were treated with 10ng/ml of TWEAK for 18h following isolation of total RNA enriched with small RNAs. [score:4]
miR-148b −2.6183 decrease apoptosis miR-152 −2.3341 Increase cell growth miR-17 −6.2545 Bcl2, N-myc miR-181c −3.5756 proliferation and remo deling of muscles miR-190b −2.2 Binds to Ubiquitin-specific protease 46, increase cell growth miR-192 −2.4871 Increase cell growth miR-199a-3p −1.9 Activin receptor IIA, Map3k4 miR-218-1 −2.2887 Increase cell growth miR-23b −2.1623 Increase Cell growth, proliferation miR-26a −2.4565 decrease proapoptotic signaling miR-27a −2.7 Ubiquitin-conjugating enzyme E2N miR-27b −3 Ubiquitin-conjugating enzyme E2N miR-296-3p −7.3378 Increase cell growth, decrease apoptosis miR-322 8.7 Hydroxysteroid (17-beta) dehydrogenase 7 miR-455 129.249 Up-regulated brown adipocyte differentiation miR-470 3.2 TGFB -induced factor homeobox 1 miR-715 18.25 Fucosyltransferase 1 miR-7a −6.2174 Increase cell growth, decrease apoptosis miR-93 −48.423 Map3k14 (NIK) miR-98 1.8 Tripartite motif-containing 6, insulin-like growth factor 2 mRNA binding protein 1 In order to understand the interaction between different genes, we generated common networks using Ingenuity Pathway Analysis (IPA) software. [score:4]
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[+] score: 17
IPost up-regulated miR-1, miR-15b, miR-21, miR-24, miR-26a, miR-27, miR-133a, miR-199a, miR-214, miR-208 and miR-499, while down-regulated miR-23a and miR-9 as compared with Sham group. [score:6]
Compared with sham group, the expressions of miR-1, miR-15b, miR-21, miR-24, miR-26a, miR-27, miR-133a, miR-199a, miR-214, miR-208 and miR-499 were increased in IPost hearts, while miR-9 and miR-23a were down-regulated in IPost mo dels. [score:5]
Then real-time quantitative PCR was performed to quantify the expression level of miR-1, miR-9, miR-15b, miR-21, miR-23a, miR-24, miR-26a, miR-27, miR-133a, miR-199a, miR-208, miR-214 and miR-499 with SYBR Green PCR Master Mix (Applied Biosystems) according to the manufacturer’s instructions. [score:3]
As previously reported, a collection of miRNAs were abnormally expressed in ischemic mouse hearts in response to I/R injury, such as miR-1, miR-9, miR-15b, miR-21, miR-23a, miR-24, miR-26a, miR-27, miR-133a, miR-199a, miR-208, miR-214 and miR-499 [20, 21, 28]. [score:3]
[1 to 20 of 4 sentences]
19
[+] score: 17
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-17, hsa-mir-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-27a, hsa-mir-30a, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-107, mmu-let-7g, mmu-let-7i, mmu-mir-30a, mmu-mir-30b, mmu-mir-125b-2, mmu-mir-9-2, mmu-mir-150, mmu-mir-24-1, mmu-mir-204, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-204, hsa-mir-210, hsa-mir-221, hsa-mir-222, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125b-2, hsa-mir-150, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-21a, mmu-mir-24-2, mmu-mir-27a, mmu-mir-103-1, mmu-mir-103-2, mmu-mir-326, mmu-mir-107, mmu-mir-17, mmu-mir-210, mmu-mir-221, mmu-mir-222, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-125b-1, hsa-mir-30c-1, hsa-mir-30e, hsa-mir-378a, mmu-mir-378a, hsa-mir-326, ssc-mir-125b-2, ssc-mir-24-1, ssc-mir-326, ssc-mir-27a, ssc-let-7c, ssc-let-7f-1, ssc-let-7i, ssc-mir-103-1, ssc-mir-107, ssc-mir-204, ssc-mir-21, ssc-mir-30c-2, ssc-mir-9-1, ssc-mir-9-2, hsa-mir-378d-2, hsa-mir-103b-1, hsa-mir-103b-2, ssc-mir-15a, ssc-mir-17, ssc-mir-30b, ssc-mir-210, ssc-mir-221, ssc-mir-30a, ssc-let-7a-1, ssc-let-7e, ssc-let-7g, ssc-mir-378-1, ssc-mir-30d, ssc-mir-30e, ssc-mir-103-2, ssc-mir-27b, ssc-mir-24-2, ssc-mir-222, ssc-mir-125b-1, hsa-mir-378b, hsa-mir-378c, ssc-mir-30c-1, ssc-mir-378-2, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, mmu-mir-378b, ssc-let-7a-2, hsa-mir-378j, mmu-mir-21b, mmu-let-7j, mmu-mir-378c, mmu-mir-21c, mmu-mir-378d, mmu-mir-30f, ssc-let-7d, ssc-let-7f-2, ssc-mir-9-3, ssc-mir-150-1, ssc-mir-150-2, mmu-let-7k, ssc-mir-378b, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
Cai et al. (2014) found that 18 miRNAs were differentially expressed between intact and castrated male pigs, including miR-15a, miR-21, miR-27, miR-30, and so on [23]; Bai et al. (2014) reported that 177 miRNAs had more than 2-fold differential expression between castrated and intact male pigs, including miR-21, miR-30, miR-27, miR-103, and so on [22]. [score:5]
These indicated that miR-21, miR-30, and miR-27 and their target lncRNAs may play an important role in the androgen deficiency-related fat deposition, as it is wi dely known that miR-30a targets the androgen receptor (AR) gene [22]. [score:5]
Five depressing-adipogenesis miRNAs (miR-27, miR-150, miR-221, miR-222, and miR-326) target 217 lncRNAs. [score:3]
Our results were consisted with these reports, it was predicted that there were lncRNAs were the target genes for miR-21, miR-30, and miR-27. [score:3]
We analyzed the relationship between the 343 identified lncRNAs with the 13 promoting adipogenesis miRNAs (let-7、miR-9、miR-15a、miR-17、miR-21、miR-24、miR-30、miR-103、miR-107、miR-125b、miR-204、miR-210、and miR-378) and five depressing adipogenesis miRNAs (miR-27, miR-150, miR-221, miR-222, and miR-326). [score:1]
[1 to 20 of 5 sentences]
20
[+] score: 16
miR-24 remained significantly downregulated at three time points (days 7, 14 and 28; Fig. 1d), while miR-23b and miR-27b were downregulated only at day 7, supporting independent release of individual miRNAs from the cluster-transcript. [score:7]
miR-27b was also downregulated in AAA (Fig. 6c). [score:4]
It also causes a transient minor increase in miR-27b expression (Supplementary Fig. 7B). [score:3]
Pri-miR-23b, -27b and -24-1 may be transcribed independently from the cluster gene in mice, although pre-miR-23b may be co-transcribed with pre-miR-27b and pre-miR-24-1 (ref. [score:1]
One is intronic (mouse-chr13; human-chr9: miR-23b, miR-27b and miR-24-1) and the second is intergenic (mouse-chr8; human-chr19: miR-23a, miR-27a and miR-24-2) 12. [score:1]
[1 to 20 of 5 sentences]
21
[+] score: 15
Nevertheless, the Cryptosporidium parvum infection, a protozoan parasite that infects the gastrointestinal epithelium, causes miR-27b upregulation that suppresses KH-type splicing regulatory protein and contributed to epithelial production of NO, helping the epithelial antimicrobial defense (38). [score:7]
Herein, we found an upregulation of the miR-23b~27b~24 cluster, thus at variance with the findings observed in primary macrophages, which exhibit rapid decrease miR-27a and miR-27b expression upon murine cytomegalovirus infection (37). [score:6]
Among miRNAs significantly modulated due infection, miR-27a and miR-27b, also exhibited dependence whether TEC sorted out from the thymus exhibited cortical or medullary phenotype. [score:1]
Mature miR-27a and miR-27b differ from each other by just one nucleotide and are transcribed from paralog clusters, the intergenic miR-23a~27a~24 cluster (localized in chromosome 9q22) and the intronic miR-23b~27b~24 cluster (localized in chromosome 19p13) (35, 36). [score:1]
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22
[+] score: 14
Among miRs identified in OA, miR-22 targets BMP7, a factor inducing chondrocyte terminal differentiation [18]; miR-140 targets HDAC4, a histone deacetylase inducer of chondrocyte terminal differentiation [19, 20]; and miR-27b targets MMP13, a key remo deling enzyme in hypertrophic terminally differentiated chondrocyte [21]. [score:7]
Remarkably, miR27b was recently shown to inhibit MMP13 expression in IL-1β -treated chondrocytes [21] and miR23a/b could negatively regulate Runx2, a transcription factor involved in chondrocyte terminal differentiation, OA, and osteoblastogenesis [54]. [score:6]
Interestingly, we found among them several previously OA -associated miRs such as miR-27b, miR-199, miR-29a, miR-26, and miR-365 [16, 17]. [score:1]
[1 to 20 of 3 sentences]
23
[+] score: 14
To validate the microarray results, the expressions of five miRNAs were quantified using real-time quantitative PCR, including two up-regulated (miR-23a-3p and miR-215-5p) and three down-regulated (miR-27b-3p, miR-101a-3p, and miR-6394) miRNAs (Fig.   2d). [score:9]
Only 15 miRNAs from the 64 DEMs had validated target genes in IPA by target filter analysis, including miR-6349, miR-101a-3p, miR-6394, miR-126a-3p, miR-721, miR-143-3p, miR-497a-5p, miR-93-5p, miR-215-5p, miR-199a-3p, miR-23a-3p, miR-27b-3p, miR-2861, miR-30a-5p, and miR-370-3p. [score:5]
[1 to 20 of 2 sentences]
24
[+] score: 13
Furthermore, to determine which miRNAs can suppress endogenous KSRP mRNA expression, NIH-3T3 cells were singularly transfected with let-7b, let-7c, miR-24 or miR-27b mimic and the steady-state KSRP expression level was assayed by western blot and quantitative RT-PCR. [score:6]
Eight candidate miRNAs targeting KSRP 3′UTR were predicted by these programs (Figure S4A), but only let-7b, let-7c, miR-24, miR-27a, and miR-27b were expressed during pituitary development, as evaluated by a miRNA profiling array experiment (Table S2). [score:4]
miRNA mimics for control, let-7b, let-7c, miR-24, and miR-27b (Qiagene) as well as miRNA inhibitors for control, let-7b, let-7c, miR-24, and miR-27b (Qiagene) were singularly transfected at 100 nM final concentration. [score:3]
[1 to 20 of 3 sentences]
25
[+] score: 13
Figure 4 A. Histograms of individual miRNA QPCR analysis showing circulating levels of randomly selected miRNAs (miR-20a, miR-27b, miR-1224-3p, miR-1260, and miR-93) in the serum of animals with non-metastatic primary disease or with high-risk metastatic disease. [score:5]
Compared with the non-metastatic favorable disease animals, we observed marginal variations in the expression of miR-20a, miR-27b, miR-93, miR-1260, and miR-1224 (Figure 4A). [score:4]
For the present study, we used QPCR to confirm expression of selected miRNAs, including hsa-miR-1224-3p, hsa-miR-1260, hsa-miR-27b, hsa-miR-93, and hsa-miR-20a. [score:3]
B. Correlation analysis of the serum-circulating profiles of miR-20a, miR-27b, miR-1224-3p, miR-1260, and miR-93 observed using the miRnome approach. [score:1]
[1 to 20 of 4 sentences]
26
[+] score: 13
In addition, developmental upregulation of some miRNAs identified in our screen was observed in differentiating oligodendrocytes in vitro, including miR-146, miR-23b, miR-24, and miR-27b in one study [13] and miR-204, miR-27b and miR-100 very recently in another study [20]. [score:5]
Furthermore, miRNAs were confirmed to be upregulated upon myelination: p≤0.0001 (miR-34a, miR-146b), p = 0.04 (miR-338-3p), p = 0.003 (miR-204), p = 0.0007 (miR-27b), p = 0.005 (miR-140), p = 0.0002 (miR-138), p = 0.01 (miR-195), p = 0.0004 (miR-30a). [score:4]
All miRNAs analyzed were significantly downregulated in Dicer [fl/fl] Dhh-Cre [+] nerves at p4: p≤0.0001 (miR-34a, miR-146b, miR-338-3p, miR-204, miR-27b, miR-140, miR-138, miR-30a), p = 0.0002 (miR-195). [score:4]
[1 to 20 of 3 sentences]
27
[+] score: 12
Our data also documented a statistically significant up-regulation of miR-23b cluster miRNAs (miR-23b, miR-27b, and miR-24) during postnatal aortic development (Supplementary Table S2), consistent with an inhibitory effect of these miRNAs on TGF- signaling. [score:7]
As with miR-29 and miR-145, computational analysis of the target gene profile for miR-27 and miR-24 showed a significant shift in the aortic samples from six-week old mice (Fig. 2), suggesting that these miRNAs also contribute to the mRNA expression profile in the adult aorta. [score:5]
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28
[+] score: 12
Furthermore, overexpression of miR-27b* suppressed LPS -induced activation of NF- κB [32]. [score:5]
MiR-27b, miR-214, miR-199a-3p, miR-182, miR-183, miR-200a, and miR-322 were found to be downregulated, whereas miR-705 and miR-1224 were increased after 4 weeks of alcohol feeding in mice [26]. [score:4]
In line with this, miR-27a*, miR-27b*, miR-29b*, miR-24-2*, and miR-21* were reported to be differentially expressed in response to H [2]O [2] -induced oxidative stress in RAW 264.7 macrophage [32]. [score:3]
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29
[+] score: 12
Promoter-reporter experiments supported the idea that miR-155, miR-186, miR-24, miR-27b, or miR-375 bind to the 3′UTR of Gabra4 and thereby inhibit protein production. [score:3]
Several bioinformatic databases and prediction algorithms showed that the selected miRNAs (miR-155, miR-186, miR-24, miR-27b, and miR-375) have a large number of potential target genes including Gabra4. [score:3]
miR-27b expression was not altered in this study, but it has a poorly conserved seed match among vertebrates at positions 331–337 (Fig. 9). [score:3]
Cortical neurons were cotransfected with pMIR-Gal + pMIR-Luc (Gal/Luc), pMIR-Gal + pMIR-Luc-3′UTR in the absence (Gal/Luc-3′UTR) or presence of scrambled oligo (Gal/Luc-3′UTR + Scr) or mimic of miR-155 (m155), miR-186 (m186), miR-24 (m24), miR-27b (m27b), or miR-375 (m375). [score:1]
miR-155, miR-186, miR-24, miR-27b, and miR-375 have predicted binding sites along the 3′UTR of Gabra4 (1965 bp, NM_010251) (www. [score:1]
Figure 7Transfection of miR-155, miR-186, miR-24, miR-27b, or miR-375 mimics decreases luciferase activity and Gabra4 protein levels in cultured mouse cortical neurons. [score:1]
[1 to 20 of 6 sentences]
30
[+] score: 11
Interestingly, both Drosha and DGCR8 appear to be targeted by p53-miR, miR-27, while both Dicer and TARBP2 appear to be targeted by p53-miRs, such as let-7, miR-103/107, and miR-15/16/195, suggesting a co-ordinated regulation of miRNA processing mediated by the p53-miRs. [score:6]
Among the p53-miRs that target the components of the miRNA processing complexes, miR-15/16/195, miR-103, miR-107, let-7, miR-124, miR-181, miR-148a/b, miR-30a/c, miR-27, miR-17, and miR-20 appear to target more than five components of the miRNA-processing pathway [Table 4, Table S3], suggesting the conserved nature of p53-miRs. [score:5]
[1 to 20 of 2 sentences]
31
[+] score: 11
So miR-27-3p represses Wnt3a protein expression to inhibit melanogenesis. [score:5]
In conclusion, our results demonstrated that Wnt3a is a target of miR-27-3p, and miR-27a-3p can inhibit melanogenesis in melanocytes. [score:5]
To determine the effect of miR-27-3p on the production of melanin in melanocytes, the melanin contents in the cells transfected with miR-27a-3p mimic or miR-27a-3p inhibitor, as well as their negative controls were measured. [score:1]
[1 to 20 of 3 sentences]
32
[+] score: 11
Highest-ranking miRNAs included miR-16/15a (46 targets), miR-27b (44 targets), let-7f (35 targets), miR-26b (33 targets), and miR-25 (30 targets). [score:11]
[1 to 20 of 1 sentences]
33
[+] score: 11
In Piedmontese cattle with mutated myostatin gene, MSTN gene was found to be targeted by miR-27b and miR-27b expression was correlated with hypertrophic phenotype of Piedmontese cattle [46]. [score:5]
In addition to well-known myomiRs, recent studies have demonstrated that miR-486 [49], miR-378 [50], miR181a [80], miR-21a, miR-101a, and miR-151 [54] are also involved in regulation of myogenesis and several other ubiquitously expressed miRNAs have also been found to participate in myogenesis, including miR-26a [51], miR-27b [52, 53], and miR-29 [44]. [score:4]
Two other myomiRs, miR-26a, and miR-27b were high-count sequences in both libraries of transgenic and wild-type mice. [score:1]
MiR-133a [23, 38], miR-378a [50], miR-26a [51], miR-27b [52, 53], miR-21a [56], miR-29a [44], miR-148 [58], and miR-103 are skeletal muscle specific miRNAs and play a vital role in muscle differentiation and proliferation as reported in previous studies. [score:1]
[1 to 20 of 4 sentences]
34
[+] score: 10
Other miRNAs from this paper: hsa-mir-27a, hsa-mir-27b, mmu-mir-27a
Reduced miR-27 was shown to directly target key components of brown adipose transcription, such as Pparα and Creb1 [46]. [score:4]
Possibly, since miR-27 is downregulated following prolonged cold exposure, and HD mice show progressive hypothermia [38], altered levels of miR-27 in HD mice could be involved in browning of their WAT. [score:4]
A recent study highlighted miR-27 as a transcriptional regulator of brown adipogenesis [46]. [score:2]
[1 to 20 of 3 sentences]
35
[+] score: 10
Overexpression of miR-27b causes premature differentiation of muscle satellite cells: once myoblasts exit the cell cycle, miR-27 indeed targets the 3'UTR of Pax3 (Crist et al., 2009). [score:5]
Muscle stem cell behavior is modified by microRNA-27 regulation of Pax3 expression. [score:4]
Specific miRNAs are critical for satellite cell activation (miR-27b) or for skeletal muscle differentiation (miR-1) and can be induced for therapeutic approaches. [score:1]
[1 to 20 of 3 sentences]
36
[+] score: 10
0034688.g009 Figure 9 The mature form of miRNAs: miR-17, miR-21, miR-27 and miR-93 were up-regulated, as were their underlying pri-miRNAs in the old (O) vs. [score:4]
0034688.g010 Figure 10 The mature form of miRNAs: miR-17, miR-21, miR-27 and miR-93 were up-regulated, as were their underlying pri-miRNAs in the old (O) vs. [score:4]
As shown in Figure 9, the miRNA guide strand miR-17, miR-21, miR-27a and miR-93 had an age-related increase accordingly with their corresponding primary transcripts pri-mir-17, pri-mir-21, pri-mir-27 and pri-mir-93. [score:1]
miR-23a, miR-27b were also induced during early hypertrophic growth in response to pressure-overload [53], [54]. [score:1]
[1 to 20 of 4 sentences]
37
[+] score: 10
Natural compounds such as persimmon tannin have been shown to inhibit the differentiation of 3T3-L1 cells through upregulation of miR-27a and miR-27b [24]. [score:6]
Among them, miR-27a and miR-27b have been reported as negative regulators of adipocyte differentiation through peroxisome proliferator-activated receptor gamma (PPARγ) inhibition [23]. [score:4]
[1 to 20 of 2 sentences]
38
[+] score: 10
In contrast, the M1 activator LPS upregulates miR-27b to silence PPARγ expression in M1 macrophages 17, thus inhibiting M2 gene expression. [score:10]
[1 to 20 of 1 sentences]
39
[+] score: 9
Other miRNAs from this paper: mmu-mir-133a-1, mmu-mir-133a-2
This effect may be mediated by the NO -dependent regulation of both miR-133a, a known regulator of collagen 1A1 expression [55], and miR-27b, a key inhibitor of adipocyte differentiation that controls the expression of peroxisome proliferator-activated receptor γ [56]. [score:9]
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40
[+] score: 9
For example, miR-106b, miR-21, miR- 22, miR-19b and miR-25 are known to regulate PTEN and miR-27 and miR-139 repress FoxO1 translation through direct binding to the 3′-UTR [31], [32], [33], [34], [35], [36], [37], [38]. [score:5]
Among the up-regulated miRNAs, miR-106b, miR-25 and miR-19b share the same primary transcripts, and miR-24 and miR-27 share primary transcripts. [score:4]
[1 to 20 of 2 sentences]
41
[+] score: 9
Other miRNAs from this paper: hsa-mir-27b
Human MSC applied systemically were found in the liver potentially mediated by mir-27b down-regulation in liver and up-regulation of SDF1 expression. [score:9]
[1 to 20 of 1 sentences]
42
[+] score: 9
Other miRNAs from this paper: mmu-mir-10b
[31] An HGF -dependent downregulation of miR-27b and upregulation of the target ST14/matriptase is proposed. [score:9]
[1 to 20 of 1 sentences]
43
[+] score: 8
miR-27a and miR-27b regulate autophagic clearance of damaged mitochondria by targeting PTEN -induced putative kinase 1 (PINK1). [score:4]
MiR-27a and miR-27b regulate autophagic clearance of damaged mitochondria by targeting PINK1 (Kim et al., 2016). [score:4]
[1 to 20 of 2 sentences]
44
[+] score: 8
Other miRNAs tested, miR-27 and miR-25/32/92/363/367 have highly conserved binding sites but did not have an effect on reporter gene expression in HEK293 or 501mel cells. [score:3]
The other miRNAs tested, miR-27, miR-32 and miR-101 did not show significant effects on luciferase expression in this assay (Fig. 2B). [score:2]
All Mitf 3′UTR sequences in 11 vertebrate species analysed contain the miR-27, miR-25/32/92/363/367 and the miR-101/144 binding sites (Fig. 1B). [score:1]
Black bars: miR-124/506 binding sites, dark grey bars: binding sites, light grey bars: miR-148/152 binding sites, white bars: miR-27, miR-25/32/92/363/367 and miR-101/144. [score:1]
A. The line indicates the 3′ UTR region of the mouse Mitf gene, including the coding region of exon 9. Potential binding sites for miR-27, miR-124/506, miR-25/32/92/363/367, miR-148/152, and miR-101/144 in the mMitf 3′UTR sequence are indicated below the line and potential PAS sites above. [score:1]
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45
[+] score: 8
As a consequence, several of the miR-27 target genes, including Prdm16, peroxisome proliferator-activated receptor alpha (Pparα), cAMP response element -binding protein (Creb) and peroxisome proliferator-activated receptor gamma coactivator 1-beta (Pgc1β) are upregulated, and enhance brown adipogenesis. [score:6]
Several miRNAs controlling mouse brown adipocyte development and function have been identified in mice, including miR-27, −34a, −133, −155, −182, −193b-365, −196, −203 and miR-378 [14, 16– 23]. [score:2]
[1 to 20 of 2 sentences]
46
[+] score: 8
As such affector miRNAs, that act independently from the interaction of Nrf2 with Keap1, miRNAs miR-153, miR-27-a, miR-142-5p, and miR-144 regulated the Nrf2 expression in neuroblastoma cells [179], and miR-28 targeted the 3’UTR of Nrf2 mRNA decreasing Nrf2 expression in human breast cancer cells [180]. [score:8]
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47
[+] score: 8
Ji and colleagues determined that both miR-27a and miR-27b target the 3′-UTR of the retinoid X receptor α and play a similar role in regulating fat metabolism and cell proliferation during rat hepatic stellate cell activation (35). [score:4]
Recent studies mentioned that miR-27a and miR-27b play an important role in macrophage polarization by targeting the 3′-UTR of IRF4 (23). [score:3]
Early studies reported that miR-27a and miR-27b have antiviral activities against murine cytomegalovirus infection in different mouse cell lines (34). [score:1]
[1 to 20 of 3 sentences]
48
[+] score: 7
At 6 h, 40 miRNAs were upregulated (such as miR-146b-5p, miR-27b-3p and let-7f-5p) and 20 were downregulated (such as miR-127-5p, miR-3094-3p and miR-30c-1-3p) (Figure 3B; Table 1). [score:7]
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49
[+] score: 7
The latter includes the well-characterized miR-17_92 cluster, which targets several tumor suppressors and is enriched in many types of cancer (for a review, see [29]), but also members of the miR-27 family, which suppresses expression of the breast cancer marker CYP1B1 [30]. [score:7]
[1 to 20 of 1 sentences]
50
[+] score: 7
miR-27 tumor suppressor functional studies. [score:3]
SGPP1 and Smad2 were overpressed in human colorectal cancer cells and cancer tissues, which were inversely correlated with miR-27 expression. [score:3]
C, miR-27 levels in tumors from untreated (NC) and miR-27a treated groups were validated by qRT-PCR. [score:1]
[1 to 20 of 3 sentences]
51
[+] score: 7
However, previous studies on hMSCs-Ad undergoing adipogenesis reported that miR-21 13, miR-22 14, miR-196 15, miR-27b 20, and miR-138 31 were either upregulated or downregulated, and miR-148a was not reported in hMSCs-Ad. [score:7]
[1 to 20 of 1 sentences]
52
[+] score: 7
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-107, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-23b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-125a, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-136, mmu-mir-138-2, mmu-mir-181a-2, mmu-mir-24-1, mmu-mir-191, hsa-mir-196a-1, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-122, mmu-mir-143, mmu-mir-30e, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-196a-2, hsa-mir-181a-1, mmu-mir-296, mmu-mir-298, mmu-mir-34c, mmu-let-7d, mmu-mir-130b, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-23b, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-138-2, hsa-mir-143, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-136, hsa-mir-138-1, mmu-mir-19b-2, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-148a, mmu-mir-196a-1, mmu-mir-196a-2, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-18a, mmu-mir-20a, mmu-mir-21a, mmu-mir-24-2, mmu-mir-29a, mmu-mir-29c, mmu-mir-27a, mmu-mir-92a-2, mmu-mir-93, mmu-mir-34a, mmu-mir-103-1, mmu-mir-103-2, mmu-mir-330, mmu-mir-346, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-107, mmu-mir-17, mmu-mir-19a, mmu-mir-100, mmu-mir-181a-1, mmu-mir-29b-2, mmu-mir-19b-1, mmu-mir-92a-1, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-34c, hsa-mir-296, hsa-mir-130b, hsa-mir-30e, hsa-mir-375, hsa-mir-381, mmu-mir-375, mmu-mir-381, hsa-mir-330, mmu-mir-133a-2, hsa-mir-346, hsa-mir-196b, mmu-mir-196b, hsa-mir-18b, hsa-mir-20b, hsa-mir-146b, hsa-mir-519d, hsa-mir-501, hsa-mir-503, mmu-mir-20b, mmu-mir-503, hsa-mir-92b, mmu-mir-146b, mmu-mir-669c, mmu-mir-501, mmu-mir-718, mmu-mir-18b, mmu-mir-92b, hsa-mir-298, mmu-mir-1b, hsa-mir-103b-1, hsa-mir-103b-2, hsa-mir-718, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-30f, mmu-let-7k, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
Another important member of this miR-23b cluster is miR-27b, which has also been shown to play important roles in adipogenesis by impairing differentiation of human adipocytes and targeting PPARγ [43]. [score:3]
However, we found that miR-27b was not robustly expressed in brown or white primary adipocytes. [score:3]
Activation of the miRNA cluster miR-17~92 enhances adipogenesis [28] while let-7 and miR-27 impair adipogenic differentiation [29, 30]. [score:1]
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[+] score: 7
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-21, hsa-mir-22, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26a-1, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-99a, mmu-let-7g, mmu-let-7i, mmu-mir-99a, mmu-mir-140, mmu-mir-10b, mmu-mir-181a-2, mmu-mir-24-1, mmu-mir-191, hsa-mir-192, hsa-mir-148a, hsa-mir-30d, mmu-mir-122, hsa-mir-10b, hsa-mir-181a-2, hsa-mir-181a-1, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-122, hsa-mir-140, hsa-mir-191, hsa-mir-320a, mmu-mir-30d, mmu-mir-148a, mmu-mir-192, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-21a, mmu-mir-22, mmu-mir-24-2, mmu-mir-26a-1, mmu-mir-92a-2, mmu-mir-25, mmu-mir-181a-1, mmu-mir-26a-2, mmu-mir-92a-1, hsa-mir-26a-2, hsa-mir-423, hsa-mir-451a, mmu-mir-451a, hsa-mir-486-1, mmu-mir-486a, mmu-mir-423, bta-mir-26a-2, bta-let-7f-2, bta-mir-148a, bta-mir-21, bta-mir-30d, bta-mir-320a-2, bta-mir-99a, bta-mir-181a-2, bta-mir-27b, bta-mir-140, bta-mir-92a-2, bta-let-7d, bta-mir-191, bta-mir-192, bta-mir-22, bta-mir-423, bta-let-7g, bta-mir-10b, bta-mir-24-2, bta-let-7a-1, bta-let-7f-1, bta-mir-122, bta-let-7i, bta-mir-25, bta-let-7a-2, bta-let-7a-3, bta-let-7b, bta-let-7c, bta-let-7e, hsa-mir-1246, bta-mir-24-1, bta-mir-26a-1, bta-mir-451, bta-mir-486, bta-mir-92a-1, bta-mir-181a-1, bta-mir-320a-1, mmu-mir-486b, hsa-mir-451b, bta-mir-1246, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-451b, mmu-let-7k, hsa-mir-486-2
There were eight microRNAs (bta-miR-27b, bta-miR-191, bta-miR-30d, bta-miR-451, bta-miR-25, bta-miR-140, bta-miR-24-3p, and bta-miR-122), that were upregulated in older animals in the present study, and upregulated in fetal muscle tissue of the study. [score:7]
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Other miRNAs from this paper: hsa-let-7c, hsa-let-7d, hsa-mir-16-1, hsa-mir-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-28, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-99a, hsa-mir-101-1, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-30a, mmu-mir-99a, mmu-mir-101a, mmu-mir-125b-2, mmu-mir-126a, mmu-mir-128-1, mmu-mir-9-2, mmu-mir-142a, mmu-mir-144, mmu-mir-145a, mmu-mir-151, mmu-mir-152, mmu-mir-185, mmu-mir-186, mmu-mir-24-1, mmu-mir-203, mmu-mir-205, hsa-mir-148a, hsa-mir-34a, hsa-mir-203a, hsa-mir-205, hsa-mir-210, hsa-mir-221, mmu-mir-301a, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-125b-1, hsa-mir-128-1, hsa-mir-142, hsa-mir-144, hsa-mir-145, hsa-mir-152, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125b-2, hsa-mir-126, hsa-mir-185, hsa-mir-186, mmu-mir-148a, mmu-mir-200a, mmu-let-7c-1, mmu-let-7c-2, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-21a, mmu-mir-24-2, mmu-mir-29a, mmu-mir-31, mmu-mir-34a, mmu-mir-148b, mmu-mir-339, mmu-mir-101b, mmu-mir-28a, mmu-mir-210, mmu-mir-221, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-125b-1, mmu-mir-128-2, hsa-mir-128-2, hsa-mir-200a, hsa-mir-101-2, hsa-mir-301a, hsa-mir-151a, hsa-mir-148b, hsa-mir-339, hsa-mir-335, mmu-mir-335, hsa-mir-449a, mmu-mir-449a, hsa-mir-450a-1, mmu-mir-450a-1, hsa-mir-486-1, hsa-mir-146b, hsa-mir-450a-2, hsa-mir-503, mmu-mir-486a, mmu-mir-542, mmu-mir-450a-2, mmu-mir-503, hsa-mir-542, hsa-mir-151b, mmu-mir-301b, mmu-mir-146b, mmu-mir-708, hsa-mir-708, hsa-mir-301b, hsa-mir-1246, hsa-mir-1277, hsa-mir-1307, hsa-mir-2115, mmu-mir-486b, mmu-mir-28c, mmu-mir-101c, mmu-mir-28b, hsa-mir-203b, hsa-mir-5680, hsa-mir-5681a, mmu-mir-145b, mmu-mir-21b, mmu-mir-21c, hsa-mir-486-2, mmu-mir-126b, mmu-mir-142b, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
In a number of single studies, miRNAs such as let-7d [26], let-7i [26] and miR-210 [23] were also found to be up-regulated in prostate cancer, in contrast to let-7g [23], miR-27b [28], miR-99a [23], miR-126 [54], miR-128 [26], miR-152 [28], miR-200a [58] and miR-449a [59] which were down-regulated in prostate cancer samples. [score:7]
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A total of 11 miRNAs, let-7, miR-9, miR-206, miR-138, miR-133, miR-152, miR-137, miR-128, miR-143, miR-27b and miR-218 were co-expressed by 18 synaptic transmission target genes (Table S6). [score:5]
For synaptic transmission, miR-128, miR-27b, miR-133, miR-206, miR-152 and miR-9 are shared between development and tumor using picTar prediction; miR-128, miR-140, miR-27b, miR-22, miR-133, miR-223 and miR-152 are shared using PITA prediction. [score:2]
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[+] score: 6
In the non-alcoholic fatty liver disease mo del, the treatment with a dietetic regimen, which caused various liver injuries, demonstrated that there was significant downregulation of miR-451 and miR-27 in the livers of these rats 45. [score:6]
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[+] score: 6
Other miRNAs from this paper: mmu-mir-10b, mmu-mir-34c, mmu-mir-34b, mmu-mir-34a
Second, other miRNAs may also repress MCM expression, as we showed was the case for miR-27b and 181a. [score:3]
Mcm2-7 mRNA levels were not reduced after miR-10b, 181a or 27b over -expression (S5B Fig), while miR-27b and 181a repressed MCM4 but not other MCMs studied (Fig 6F). [score:3]
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58
[+] score: 6
Zhu J et al. found that Downregulation of microRNA-27b-3p enhances tamoxifen resistance in breast cancer by increasing NR5A2 and CREB1 expression [29]. [score:6]
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[+] score: 6
Interestingly, Fasn and Scd1 were found to be promising targets of miR-27a and miR-27b in sequence alignments (Fig.   1a,b). [score:3]
Vickers et al. reported that miR-27b is a regulatory hub in hepatic lipid metabolic networks [33]. [score:2]
The seed regions of miR-27a and miR27b are indicated in bold. [score:1]
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For example, the expression of miR-27, -335, and -519d is up-regulated in liver and/or adipose tissue of obese mice or humans [32], [33], [34], [35], [36]. [score:6]
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[+] score: 6
Other miRNAs from this paper: hsa-mir-27b
Kong X, Yu J, Bi J, Qi H, Di W, Wu L, Wang L, Zha J, Lv S, Zhang F, Li Y, Hu F, Liu F, Zhou H, Liu J, Ding G Glucocorticoids transcriptionally regulate miR-27b expression promoting body fat accumulation via suppressing the browning of white adipose tissue. [score:6]
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[+] score: 6
However expression of miR-23b and miR-27b was highest in the double negative fraction with lowest levels expressed in the T [+] (GFP [+])/Flk1 [+] fraction. [score:5]
Q-RT-PCR was performed with RNA extracted from the isolated fractions to examine the relative levels of mature mirn23a/ mirn23b miRNAs: miR-24, mir-23a, miR23b, miR-27a, and miR-27b (Fig. 7B, 7C). [score:1]
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[+] score: 6
In addition, miR-27 has been implicated in the regulation of several tumor suppressors, such as FBW7, which is involved in cyclin E degradation and cell cycle progression [42], and FOXO1, which is a transcription factor that controls the genes involved in the apoptotic response and cell cycle checkpoints in breast cancer cells [43]. [score:4]
The miR-27 family has been implicated in the development of cardiac hypertrophy, although it remains unclear how these molecules modulate growth of cardiomyocytes in response to different stimuli. [score:2]
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[+] score: 6
Finally, miR-27b regulates CYP1B1 expression post-transcriptionally in cancer tissues (Tsuchiya et al., 2006; Chuturgoon et al., 2014). [score:4]
Fumonisin B1 modulates expression of human cytochrome P450 1b1 in human hepatoma (Hepg2) cells by repressing Mir-27b. [score:2]
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We analyzed expression of miR-27b, miR-29b, miR-155, miR-124 and miR-223 in bone marrow-derived mouse macrophages differentiated in M0 (unstimulated), M1(LPS + IFN-γ) and M2(IL-4) conditions. [score:3]
miRNA expression was determined by Taqman Real-Time PCR using miR-27, miR-29b, miR-155, miR-223, miR-124 and sno-202 primer and probe sets (Life Technologies), according to manufacturer’s instructions. [score:2]
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Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-mir-15a, hsa-mir-18a, hsa-mir-33a, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-107, mmu-mir-126a, mmu-mir-128-1, mmu-mir-140, mmu-mir-146a, mmu-mir-152, mmu-mir-155, mmu-mir-191, hsa-mir-10a, hsa-mir-211, hsa-mir-218-1, hsa-mir-218-2, mmu-mir-297a-1, mmu-mir-297a-2, hsa-mir-27b, hsa-mir-128-1, hsa-mir-140, hsa-mir-152, hsa-mir-191, hsa-mir-126, hsa-mir-146a, mmu-let-7a-1, mmu-let-7a-2, mmu-mir-15a, mmu-mir-18a, mmu-mir-103-1, mmu-mir-103-2, mmu-mir-342, hsa-mir-155, mmu-mir-107, mmu-mir-10a, mmu-mir-218-1, mmu-mir-218-2, mmu-mir-33, mmu-mir-211, hsa-mir-374a, hsa-mir-342, gga-mir-33-1, gga-let-7a-3, gga-mir-155, gga-mir-18a, gga-mir-15a, gga-mir-218-1, gga-mir-103-2, gga-mir-107, gga-mir-128-1, gga-mir-140, gga-let-7a-1, gga-mir-146a, gga-mir-103-1, gga-mir-218-2, gga-mir-126, gga-let-7a-2, gga-mir-27b, mmu-mir-466a, mmu-mir-467a-1, hsa-mir-499a, hsa-mir-545, hsa-mir-593, hsa-mir-600, hsa-mir-33b, gga-mir-499, gga-mir-211, gga-mir-466, mmu-mir-675, mmu-mir-677, mmu-mir-467b, mmu-mir-297b, mmu-mir-499, mmu-mir-717, hsa-mir-675, mmu-mir-297a-3, mmu-mir-297a-4, mmu-mir-297c, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, mmu-mir-466c-1, mmu-mir-466e, mmu-mir-466f-1, mmu-mir-466f-2, mmu-mir-466f-3, mmu-mir-466g, mmu-mir-466h, mmu-mir-467c, mmu-mir-467d, mmu-mir-466d, hsa-mir-297, mmu-mir-467e, mmu-mir-466l, mmu-mir-466i, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-467f, mmu-mir-466j, mmu-mir-467g, mmu-mir-467h, hsa-mir-664a, hsa-mir-1306, hsa-mir-1307, gga-mir-1306, hsa-mir-103b-1, hsa-mir-103b-2, gga-mir-10a, mmu-mir-1306, mmu-mir-3064, mmu-mir-466m, mmu-mir-466o, mmu-mir-467a-2, mmu-mir-467a-3, mmu-mir-466c-2, mmu-mir-467a-4, mmu-mir-466b-4, mmu-mir-467a-5, mmu-mir-466b-5, mmu-mir-467a-6, mmu-mir-466b-6, mmu-mir-467a-7, mmu-mir-466b-7, mmu-mir-467a-8, mmu-mir-467a-9, mmu-mir-467a-10, mmu-mir-466p, mmu-mir-466n, mmu-mir-466b-8, hsa-mir-466, hsa-mir-3173, hsa-mir-3618, hsa-mir-3064, hsa-mir-499b, mmu-mir-466q, hsa-mir-664b, gga-mir-3064, mmu-mir-126b, gga-mir-33-2, mmu-mir-3618, mmu-mir-466c-3, gga-mir-191
Out of the 26 miRNA/host gene pairs with coordinated expression, 11 have been found to be coordinately expressed in both, human and mouse [19], [27], [59], [61]– [64], [67]– [69], [71], [73]– [79]: mir-103/ PANK3, mir-107/ PANK1, mir-126/ EGFL7, mir-128-1/ R3HDM1, mir-140/ WWP2, mir-211/ TRPM1, mir-218-1/ SLIT2, mir-218-2/ SLIT3, mir-27b/ C9orf3, mir-33/ SREBF2, and mir-499/ MYH7B. [score:5]
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67
[+] score: 5
Similarly, miR-27 inhibits the gene expression of adenomatous polyposis coli leading β-catenin accumulation and thus Wnt activation to promote osteoblast differentiation [44]. [score:5]
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NFATs may also control genes encoding signaling molecules as variate as Ca [2+] regulators [inositol 1,4,5-trisphosphate (IP [3]) receptor (IP [3]R), regulator of calcineurin 1 (RCAN1)], growth factors (VEGF, neurotrophins), myelination genes (P0 and Krox-20), glucose regulation genes (insulin, HNF1, PDX, and GLUT2), cell cycle and death regulator/activators [p21 [Waf1], c-Myc, cyclin -dependent kinase 4 (CDK4), B-cell lymphoma 2 (Bcl-2), and cyclins A2, D1, and D2], oncogenes (Wnt, β-catenin), microRNAs (miR-21, miR-23, miR-24, miR-27, miR-125, miR-195, miR-199, and miR-224), and surfactants (sftpa, sftpb, sftpc, and abca3) [9, 65– 74]. [score:5]
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[+] score: 5
miR27 inhibits the gene expression of adenomatous polyposis coli leading β-catenin accumulation and thus Wnt signaling pathways activation to promote osteoblast differentiation[26]. [score:5]
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70
[+] score: 5
Others, including let-7f, miR-27b [6], miR-221, and miR-222 [12], have been shown to modulate angiogenesis in vitro and overexpression or inhibition of miR-378 [13], the miR-17-92 cluster [14] and miR-296 [15] affects angiogenesis in mouse engrafted tumors. [score:5]
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Among the remaining 21, two were in the set of top 20 most highly expressed miRNAs in each of the MIN6 and human datasets: miR-375+1 and miR-375-1. Many of the 5′-shifted isomiRs, such as miR-375+1, miR-375-1, and miR-27b-3p-1, were expressed at similar levels in MIN6, human beta cell, and human islet samples (Fig. 3B). [score:5]
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[+] score: 5
Other miRNAs from this paper: mmu-mir-382
Molecularly, a previous study also highlighted that miR-27b-3p could activate cell proliferation, regulate colony formation and promote tumorigenicity by targeting ROR1 in gastric cancer cells [40]. [score:4]
Further data showed the c-Src/STAT3 signaling pathway may be involved in miR-27b-3p-ROR1 -mediated tumor cell proliferation [40]. [score:1]
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73
[+] score: 4
Other miRNAs from this paper: mmu-mir-27a
We then used five miRNA prediction softwares and identified miR-27a and miR-27b as potential miRNAs which could target and regulate MCPH1 (Table S6 in File S1). [score:4]
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Only one target site was identified for miR-27b* or −128 in the CDS. [score:3]
We used software prediction programs to identify candidate binding sites of miRNAs within the EGFR gene and identified miR-7, −27a (miR-27a-3p), −27a*, −27b (miR-27b-3p), −27b* (miR-27b-5p), and −128 (Fig. 1A). [score:1]
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75
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Similarly, miR-23–miR-27–miR-24 cluster overexpression impairs TGF-β -mediated Treg induction (42). [score:3]
Moreover, miRNA (miR-31, miR-17–miR-92, and miR-23–miR-27–miR-24) antagomir treatment of T cells in vitro may be exploited to support iTreg generation, while in vivo treatment may foster pTreg generation. [score:1]
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Several studies analyzing miRNAs in milk emphasize enrichments in “immune-related” miRNAs such as miR-146b, miR-27b, and the miR-200 family (14, 17, 18, 22), which were also among the more highly expressed miRNAs in murine milk. [score:3]
Interestingly, the miRNA profile for different lactation days was similar, with the same seven miRNAs dominating each lactation day (miR-148a-3p, miR-181a-5p, miR-22-3p, miR-27b-3p, miR-30a-5p, miR-146b-5p, and miR-26a-5p) (Fig. 1, A–D). [score:1]
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77
[+] score: 4
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-17, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-32, hsa-mir-33a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-106a, mmu-let-7g, mmu-let-7i, mmu-mir-30a, mmu-mir-30b, mmu-mir-126a, mmu-mir-9-2, mmu-mir-135a-1, mmu-mir-137, mmu-mir-140, mmu-mir-150, mmu-mir-155, mmu-mir-24-1, mmu-mir-193a, mmu-mir-194-1, mmu-mir-204, mmu-mir-205, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-143, mmu-mir-30e, hsa-mir-34a, hsa-mir-204, hsa-mir-205, hsa-mir-222, mmu-let-7d, mmu-mir-106a, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-30b, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-137, hsa-mir-140, hsa-mir-143, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-126, hsa-mir-150, hsa-mir-193a, hsa-mir-194-1, mmu-mir-19b-2, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-23a, mmu-mir-24-2, mmu-mir-29a, mmu-mir-31, mmu-mir-92a-2, mmu-mir-34a, rno-mir-322-1, mmu-mir-322, rno-let-7d, rno-mir-329, mmu-mir-329, rno-mir-140, rno-mir-350-1, mmu-mir-350, hsa-mir-200c, hsa-mir-155, mmu-mir-17, mmu-mir-25, mmu-mir-32, mmu-mir-200c, mmu-mir-33, mmu-mir-222, mmu-mir-135a-2, mmu-mir-19b-1, mmu-mir-92a-1, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-7b, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-106b, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-375, mmu-mir-375, mmu-mir-133b, hsa-mir-133b, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-7b, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-17-1, rno-mir-19b-1, rno-mir-19b-2, rno-mir-23a, rno-mir-24-1, rno-mir-24-2, rno-mir-25, rno-mir-27b, rno-mir-29a, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-31a, rno-mir-32, rno-mir-33, rno-mir-34a, rno-mir-92a-1, rno-mir-92a-2, rno-mir-106b, rno-mir-126a, rno-mir-135a, rno-mir-137, rno-mir-143, rno-mir-150, rno-mir-193a, rno-mir-194-1, rno-mir-194-2, rno-mir-200c, rno-mir-200a, rno-mir-204, rno-mir-205, rno-mir-222, hsa-mir-196b, mmu-mir-196b, rno-mir-196b-1, mmu-mir-410, hsa-mir-329-1, hsa-mir-329-2, mmu-mir-470, hsa-mir-410, hsa-mir-486-1, hsa-mir-499a, rno-mir-133b, mmu-mir-486a, hsa-mir-33b, rno-mir-499, mmu-mir-499, mmu-mir-467d, hsa-mir-891a, hsa-mir-892a, hsa-mir-890, hsa-mir-891b, hsa-mir-888, hsa-mir-892b, rno-mir-17-2, rno-mir-375, rno-mir-410, mmu-mir-486b, rno-mir-31b, rno-mir-9b-3, rno-mir-9b-1, rno-mir-126b, rno-mir-9b-2, hsa-mir-499b, mmu-let-7j, mmu-mir-30f, mmu-let-7k, hsa-mir-486-2, mmu-mir-126b, rno-mir-155, rno-let-7g, rno-mir-15a, rno-mir-196b-2, rno-mir-322-2, rno-mir-350-2, rno-mir-486, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
For instance, among the 66 uniformly expressed miRNAs for which IPA assigned functions, we identified 12 candidates that have been implicated in androgen regulation, including: let-7a-5p, miR-15a-5p, miR-17-5p, miR-19b-3p, miR-23a-3p, miR-24-3p, miR-27b-3p, miR-30a-5p, miR-34a-5p, miR-140-5p, miR-193a-3p, miR-205-5p (S1 Fig). [score:4]
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78
[+] score: 4
Recently, Ma reported that miR-27b was greatly up-regulated in the lung of CHD-PAH patients and correlated well with preoperative mean pulmonary arterial pressure 52. [score:4]
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79
[+] score: 4
Patel SAA Interleukin-6 mediated upregulation of CYP1B1 and CYP2E1 in colorectal cancer involves DNA methylation, miR27b and STAT3Br. [score:4]
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80
[+] score: 4
Further, we comment on miR-27b (miR-128/-27b pair appeared on the 8 [th] rank) which was shown to be up-regulated to different degrees in the old versus young adult heart and was induced during early hypertrophic growth in response to pressure-overload [6]. [score:4]
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81
[+] score: 4
In Table 1, numerous miRNAs tied to androgen response in PCa are strikingly downregulated, such as miR-27b-3p, miR-141-3p, miR-181a-5p, miR-221-3p, and miR-375-3p. [score:4]
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82
[+] score: 4
For the up-regulated genes, 21 genes among 717 genes (0.029%) were common among PostMA, MA and SCOS, and half of these genes were miRNA (LOC100130428, LOC100131541, MALAT1, MGC24103, miR-145, miR-199a-2, miR-21, miR-27b, miR-30e, miR-32, miR-99a, miR-LET7A2, miR-LET7C, miR-LET7G, PP12719, PWAR6, SNX2, TET2, ZEB2, ZNF189 and ZNF737). [score:4]
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83
[+] score: 3
miRNA p-value Fold-Change miR-146a 1.15E-09 −4.82 miR-31 9.66E-08 −4.95 miR-155 1.97E-07 −3.82 miR-2134 2.13E-07 −2.05 miR-711 1.63E-06 −4.10 miR-3473 1.95E-06 −5.62 miR-574-3p 3.32E-06 −2.55 miR-1195 6.59E-06 2.26 miR-27a* 6.89E-06 14.92 miR-27b* 7.35E-06 2.92 miR-34c 1.80E-05 −3.43 miR-1931 3.34E-05 −2.30 miR-874 4.07E-05 −2.01 miR-196b 7.99E-05 2.59 miR-181a-1* 8.02E-05 4.15 miR-187 8.11E-05 2. 02List of miRs whose expression is altered, identified from microarray analysis by comparison of levels in TM [+] and TM [−] DCs which change >2 fold with p<0.0001. [score:3]
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84
[+] score: 3
Specific miRNAs that enhance adipocyte differentiation (miR-30c, miR-143, miR-146b, and miR-378; [21– 24]) or inhibit adipocyte differentiation (miR-27, miR-130, and miR-138; [25– 27]) have been identified. [score:3]
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85
[+] score: 3
Other miRNAs from this paper: hsa-mir-27b
This conclusion is supported by recent finding that elimination of matriptase expression in MDA-MB-231 cells may be due to the cleavage of its mRNA by miR-27b microRNA [41]. [score:3]
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86
[+] score: 3
For example, it has been demonstrated that miR-15, 16, 20a, and 20b are anti-angiogenic miRNAs targeting VEGF mRNA 37, 38, whereas the miR-17–92 cluster, miR-27b, and let-7f are thought to have pro-angiogenic properties 37, 38. [score:3]
[1 to 20 of 1 sentences]
87
[+] score: 3
Previous studies have identified miR-21, miR-27, miR-96, miR-128, miR-155 and miR-182 as oncogenes, and miR-17, miR-27, miR-125, miR-145, miR-205 and miR-206 as tumor suppressor genes [13- 15]. [score:3]
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88
[+] score: 3
Here, by sequence matching using bioinformatics analyses, we found quite a few of candidate miRNAs that target Bcl-2, including miR-429, miR-30, miR-22, miR-25, miR-32, miR-92, miR-363, miR-367, miR-99, miR-27, miR-128, etc. [score:3]
[1 to 20 of 1 sentences]
89
[+] score: 3
In addition to the finding that miRNAs as a whole are essential to proper muscle formation, individual miRNAs have been shown to play key roles in myogenesis, including species that regulate satellite cell quiescence (miR-489, [6]), promote proliferation (miR-133, miR-27 [7, 8]), promote myoblast differentiation (miR-206, miR-1, miR-486 [9– 11]), and regulate fiber type switching (miR-499, miR-208a, miR-208b [12]). [score:3]
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90
[+] score: 3
The top nine most abundant miRNAs shared between the two groups were ssc-miR-10b, ssc-miR-22-3p, ssc-miR-486, ssc-miR-26a, ssc-miR-27b-3p, ssc-miR-191, ssc-miR-378, ssc-126-5p and ssc-miR-181. [score:1]
Previous studies have demonstrated that the myomiRs miR-1, miR-133a/b, miR-206, miR-486, miR-26a, miR-27b, miR-378, miR-148a and miR-181 are highly enriched in skeletal muscle and play a key role in skeletal muscle metabolism [28, 29, 30, 31]. [score:1]
In our sequencing libraries, five of these known myomiRs (miR-486, miR-26a, miR-27b, miR-378 and miR-181) were identified with the greatest abundance, accounting for 26% and 29% of the total normalized miRNA reads in the LPS-challenged and saline -treated groups, respectively. [score:1]
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91
[+] score: 3
In addition, accumulating evidence suggests that the aberrant expressions of miRNAs, such as miR-1, miR-133, miR-23a, miR-206, miR-27, miR-628, miR-431 and miR-21 (refs 17, 18, 19, 20, 21, 22, 23, 24), contribute to muscle atrophy. [score:3]
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92
[+] score: 3
miRNA mimics (miR-27 a and miR-24), miRNA inhibitors (Anti-27a and Anti-24) and negative control molecules (Scramble) were obtained from Dharmacon (Austin, TX, USA) and transfected with DharmFECT1 (Dharmacon, Austin, TX, USA) at a final concentration of 60 nM. [score:3]
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93
[+] score: 3
Other miRNAs from this paper: mmu-mir-23b, mmu-mir-24-1, mmu-mir-23a, mmu-mir-24-2, mmu-mir-27a
MiR-27a synergizes with Akt by targeting transcription factors FoxO1 (miR-27) that is repressed by Akt phosphorylation[55, 56]. [score:3]
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94
[+] score: 3
For example, miR-27 was found to be degraded in latent Herpesvirus saimiri (HVS) infection, and as a destroyer caused T-lymphoproliferative disease in HVS-infected T cells (Chi et al., 2009). [score:3]
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95
[+] score: 3
Once again we identified a number of miRNAs whose expression appeared to be repressed at a single time point including miR-187 (1 hrs), miR-27b (6 h), miR-29c (6 h), miR-100 (6 h), miR-149 (6 h), miR-150 (6 h) and miR-154 (6 h) (Table S2). [score:3]
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96
[+] score: 3
The contradictory miRNA expression levels in tumor tissues and serum have been also demonstrated for miRNA-1, miRNA-106, miRNA-146b, miRNA-155, miRNA-17-5p, and miRNA-27 (supplementary table 1 of [23]), and this phenomenon remains unexplained and needs to be explored further. [score:3]
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97
[+] score: 3
On the basis of studies in other systems, all of the upregulated miRs are considered to be pro-apoptotic [29], particularly miR-16, miR-30a, miR-27b, miR-125b, miR-30c, miR-1, and miR-218. [score:3]
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98
[+] score: 3
Since miRNAs can have different aliases, the 10 miRNAs (Fig 1) are identified as the following for the rest of this manuscript: let-7 = let-7b, let-7a-5p = let-7c, miR-10 = miR-10b, miR-130 = miR-130a, miR-155 = miR-155, miR-27 = miR27a, miR-24-3p = miR-24, miR-17 = miR-18a, miR-15 = miR-15a, and miR-16-5p = miR-497. [score:1]
This miRNA signature consists of 10 miRNAs: miR-130, miR-27, miR-17, miR-10, miR-155, let-7a-5p, let-7, miR-24-3p, miR-15, and miR-16-5p. [score:1]
Since then, it has been discovered that a number of other miRNAs, including miR-17 [13, 19], miR-27 [19, 20, 41], miR-24 [19], miR-10 [19, 20], and let-7 [12, 19, 20], play an important role in lymphoma biology. [score:1]
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99
[+] score: 3
We found that miRNAs with higher expression in WBCs includes different miRNA families: mir-15, mir-17, mir-181, mir-23, mir-27 and mir-29 families. [score:3]
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100
[+] score: 2
In addition to miR-33a/b, miR-122, miR-370, miR-335, miR-378/378*, miR-27 and miR-125a-5p have been implicated in regulating cholesterol homeostasis, fatty acid metabolism and lipogenesis [9]. [score:2]
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