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60 publications mentioning rno-mir-30c-1

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-30c-1. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 267
Other miRNAs from this paper: rno-mir-26a, rno-mir-30c-2
Transfecting NRK-52E cells with the miR-30c inhibitor significantly suppressed E-cadherin expression and enhanced Col-I expression at the protein level but not at the mRNA level; FN and α-SMA expression did not significantly change. [score:11]
Transfection with both miR-26a and miR-30c inhibitors (each at half the dose) markedly increased Col-I and α-SMA expression but reduced E-cadherin expression at the protein level; FN expression was also increased, but this effect was not significant. [score:9]
Notably, the TGFβ1 -mediated up-regulation of fibrotic marker genes and proteins was enhanced by the individual miR-26a and miR-30c inhibitors compared with the NC+TGFβ1 group; furthermore, co -inhibition with the miR-26a and miR-30c inhibitors showed a stronger pro-fibrotic effect (Fig. 4A–I). [score:9]
However, treatment with a combination of miR-26a and miR-30c mimics decreased Snail1 mRNA and protein expression to the same level as miR-26a or miR-30c alone, indicating that no synergy exists between these two miRNAs in suppressing Snail1 expression. [score:7]
Interestingly, miR-26a mimic+TGFβ1 also decreased Snail1 mRNA and protein expression, even though Snail1 3′-UTR does not contain a miR-26a target site; however, the inhibitory effect was significantly less than that of miR-30c mimic+TGFβ1. [score:7]
For the miRNA silencing experiment, 150 nM miR-26a inhibitor, 150 nM miR-30c inhibitor or 75 nM each of miR-26a and miR-30c inhibitor (RiboBio, Guangzhou, China) was used. [score:7]
Here, we showed that silencing CTGF or Snail1 did not influence the expression of the other gene and that co-silencing both targets did not synergistically suppress TGFβ1 -induced EMT in NRK-52E cells, implying that CTGF and Snail1 are independent transcription factors that cannot explain the coordinated roles of miR-26a and miR-30c. [score:7]
Notably, in the presence of TGFβ1 and either the miR-26a or miR-30c mimic, the expression of FN, Col-I and α-SMA was markedly reduced, but E-cadherin expression was markedly increased compared with the NC+TGFβ1 group; the miR-26a and miR-30c mimics had a similar inhibitory effect on EMT. [score:6]
In addition, miR-30c mimic transfection into NRK-52E cells significantly suppressed FN and Col-I expression at the protein level but not at the mRNA level compared to the NC group and trended towards improving EMT marker (α-SMA) expression at the mRNA and protein levels but did not reach significance. [score:6]
miR-26a and miR-30c directly co-target CTGF, and miR-30c targets Snail1. [score:6]
These data demonstrate that CTGF is a genuine target of miR-26a/30c and that miR-30c also directly targets Snail1. [score:6]
In summary, we present a new regulatory mo del in renal tubular epithelial cells (Fig. 7), in which miR-26a and miR-30c form an miRNA network that synergistically modulates the TGFβ1 -mediated fibrotic response via coordinated inhibition of CTGF -dependent pathways and further inhibits the ERK1/2 and p38 MAPK signaling pathways. [score:6]
Interestingly, TGFβ1 treatment down-regulated the expression of CTDSP2 and CTDSPL, which are the miR-26a host genes, and of NF-YC, which is the miR-30c host gene. [score:6]
These findings could further explain how TGFβ1 directly down-regulates miR-26a and miR-30c. [score:5]
miR-26a and miR-30c coordinately inhibit CTGF expression, leading to decreased phosphorylation of ERK1/2 and p38. [score:5]
In our study, miR-26a and miR-30c synergistically suppressed CTGF and further inhibited the ERK1/2 and p38 MAPK signaling pathways. [score:5]
The results presented in this study indicate that miR-26a, which targets CTGF, and miR-30c, which targets CTGF and Snail1, provide significant renal protection in renal tubular epithelial cells. [score:5]
miR-26a expression was significantly increased by four-fold in extracellular vesicles after TGFβ1 treatment, but miR-30c expression did not change (Supplementary Fig. 6). [score:5]
First, the CTGF 3′-UTR containing the two putative miR-26a and miR-30c target sites and the Snail1 3′-UTR containing the putative miR-30c target site were cloned into the pMIR-REPORT plasmid. [score:5]
In addition, miR-30c can suppress Snail expression. [score:5]
CTGF is targeted by miR-26a and miR-30c, and Snail1 is targeted by miR-30c. [score:5]
Luciferase reporter plasmids were generated to assess the direct effects of miR-26a and miR-30c on their putative target sites in the 3′-UTRs of CTGF and Snail1 mRNA. [score:4]
In addition, we explored whether miR-26a and miR-30c regulate fibrosis by targeting CTGF and Snail1. [score:4]
We performed a loss-of-function study by knocking down miR-26a and miR-30c alone or in combination using miRNA inhibitors. [score:4]
miR-26a and miR-30c are down-regulated in the renal cortices of diabetic OLETF rats. [score:4]
Notably, compared to the NC group, transfection with the miR-26a/miR-30c mimics combination markedly decreased FN, Col-I and α-SMA expression, but not E-cadherin expression, at the protein level. [score:4]
For the miRNA overexpression experiment, 50 nM miR-26a mimic, 50 nM miR-30c mimic or 25 nM each of miR-26a and miR-30c mimic (RiboBio, Guangzhou, China) was used. [score:3]
Hence, miR-26a and miR-30c effectively and synergistically inhibited the TGFβ1 -induced activation of MAPKs in TGFβ1 -treated NRK-52E cells. [score:3]
To explore whether TGFβ1 influences miR-26a and miR-30c expression in extracellular vesicles, we isolated this compartment from NRK-52E cell supernatants. [score:3]
Bioinformatic analyses revealed that the miR-26a and miR-30c target sites in the 3′-UTR of CTGF are non-overlapping (Supplementary Fig. 1). [score:3]
Hence, inhibitor -induced repression of miR-26a and miR-30c levels may not drastically affect basal mRNA or protein levels. [score:3]
When transfected with the miR-26a or miR-30c mimic, the cellular miR-26a and miR-30c expression levels increased approximately 50- to 80-fold (Supplementary Fig. 3A,B). [score:3]
The miR-30c inhibitor -mediated induction of the fibrotic marker genes FN, Col-I and α-SMA was restrained by siSnail1, regardless of the presence of TGFβ1 (Fig. S4G–J). [score:3]
These data show that the miR-26a and miR-30c inhibitors coordinately increase TGFβ1 -induced EMT in NRK-52E cells. [score:3]
Decreased miR-26a and miR-30c expression in TGFβ1 -treated NRK-52E cells. [score:3]
miR-26a and miR-30c mimics synergistically suppress TGFβ1 -induced EMT. [score:3]
Furthermore, co-treatment with the miR-26a/miR-30c mimics further enhanced the inhibitory effect (Fig. 5B–D). [score:3]
The computational program TargetScan predicted that the 3′-UTR of CTGF harbors two predicted binding sites for miR-26a and miR-30c. [score:3]
NRK-52E cells were co -transfected with the miR-30c inhibitor and siSnail1. [score:3]
miR-26a and miR-30c inhibitors collaboratively enhance TGFβ1 -induced EMT. [score:3]
A recent report indicated that miR-26a and miR-30c were among the top 10 highly expressed miRNAs in urinary extracellular vesicles 39. [score:3]
Changes in miR-26a and miR-30c expression in the renal cortices of 40-week-old diabetic OLETF rats. [score:3]
Furthermore, miR-26a and miR-30c were consistently down-regulated compared with control conditions (Fig. 1D). [score:3]
The potential mechanism by which miR-26a and miR-30c synergistically suppress TGFβ1 -induced EMT. [score:3]
Therefore, we hypothesized that miR-26a and miR-30c synergistically inhibit CTGF and then restrain phosphorylation activity within the ERK1/2 and p38 MAPK signaling pathways. [score:3]
Urinary extracellular vesicle expression of miR-26a and miR-30c. [score:3]
An examination of several CTGF-related miRNAs revealed that miR-26a and miR-30c expression levels were the highest. [score:3]
Co-treatment with the miR-26a and miR-30c inhibitors enhances TGFβ1 -induced EMT. [score:3]
Co-treatment with the miR-26a and miR-30c mimics suppresses TGFβ1 -induced EMT. [score:3]
Under diabetic nephropathy conditions, the TGFβ1 level is increased, resulting in reduced miR-26a and miR-30c expression. [score:3]
In the presence or absence of TGFβ1, CTGF mRNA and protein levels were markedly reduced after treatment with either miR-26a or miR-30c mimic alone; treatment with both mimics strengthened the suppressive effects on CTGF compared with treatment with either miR-26a or miR-30c mimic alone (Fig. 2D,F). [score:2]
Next, we examined whether CTGF is necessary for the coordinated regulation of EMT by miR-26a and miR-30c. [score:2]
How to cite this article: Zheng, Z. et al. The coordinated roles of miR-26a and miR-30c in regulating TGFβ1 -induced epithelial-to-mesenchymal transition in diabetic nephropathy. [score:2]
miR-26a and miR-30c regulate TGFβ1 -induced EMT via CTGF/Snail1. [score:2]
Moreover, co-transfection of NRK-52E cells with the miR-26a/miR-30c mimic combination significantly inhibited EMT compared with transfection with either mimic alone, as determined by mRNA and protein levels (Fig. 3A–I). [score:2]
Furthermore, miR-30c mimic transfection significantly decreased Snail1 mRNA (Fig. 2E) and protein expression (Fig. 2F) compared to NC transfection with or without TGFβ1 treatment. [score:2]
These changes paralleled the decreases in the expression of miR-26a and miR-30c in the kidney cortex of OLETF rats compared with non-diabetic LETO rat controls (Fig. 6D). [score:2]
We also examined whether Snail1 is necessary for the regulation of EMT by miR-30c. [score:2]
TGFβ1 induces pro-fibrotic changes and reduces miR-26a and miR-30c levels in NRK-52E cells. [score:1]
Further analysis showed that there was no significant correlation between cystatin, urinary albumin excretion rate (UAER), serum creatinine (Scr), estimated glomerular filtration rate (eGFR) or HbA1C% and the levels of miR-26a and miR-30c. [score:1]
The two regions of the predicted binding sites for miR-26a and miR-30c were separated by the interval AAAAAA (Sangon Biotech, Shanghai, China). [score:1]
This result may partly explain the coordinated roles of miR-26a and miR-30c in DN. [score:1]
Mutated plasmids were constructed to contain two mutated seed sequences for miR-26a and miR-30c (from ACTTGA to GACGTC for the miR-26a binding site and from TGTTTAC to GACGAGT for the miR-30c binding site). [score:1]
Luciferase activity was significantly decreased when cells were transfected with the miR-30c mimic alone but did not change when the cells were transfected with the miR-26a mimic. [score:1]
These data show that the miR-26a and miR-30c mimics synergistically ameliorate TGFβ1-stimulated EMT in NRK-52E cells. [score:1]
Then, cells were co -transfected with the synthetic CTGF 3′-UTR plasmid, control plasmid (β-gal), and miR-26a or miR-30c mimic alone, a combination of miR-26a/30c mimics (each at half the dose for the single mimic treatment) or negative control mimic. [score:1]
However, there was no difference between the miR-30c mimic group and the combination miR-26a/miR-30c mimics group. [score:1]
The coordinated roles of miR-26a and miR-30c are complicated and require detailed study. [score:1]
To ascertain the impact of miR-26a and miR-30c on the ERK1/2 and p38 MAPK signaling pathways, 50 nM miR-26a mimic, 50 nM miR-30c mimic or 25 nM each of miR-26a and miR-30c mimic (RiboBio, Guangzhou, China) was applied to the cells 30 min after TGFβ1 or control treatment. [score:1]
However, there was no significant difference in miR-30c levels between DN and DM patients (Table 1). [score:1]
Consistent with our expectations, luciferase activity was significantly decreased when cells were treated with either miR-26a or miR-30c mimic alone. [score:1]
In addition, the 3′-UTR of Snail1 has one predicted binding site for miR-30c (Fig. 2A, Supplementary Figs 1 and 2). [score:1]
The mechanisms underlying the coordinated roles of miR-26a and miR-30c may stem from the cooperation between the CTGF and Snail1 transcription factors. [score:1]
Interestingly, this trend was even more dramatic with the combination of miR-26a and miR-30c mimics (Fig. 2B). [score:1]
The mutated plasmid contained a mutated miR-30c seed sequence (from TGTTTAC to CACGACT). [score:1]
Luciferase activity was also significantly decreased by the combination of the miR-26a and miR-30c mimics (Fig. 2B). [score:1]
We investigated the synergistic effect of miR-26a and miR-30c overexpression in NRK-52E cells with or without TGFβ1 treatment. [score:1]
As expected, activation of the ERK1/2 and p38 MAPK signaling pathways due to TGFβ1 treatment (30 min) was markedly attenuated by the individual miR-26a and miR-30c mimics. [score:1]
Hence, the mimic -induced promotion of miR-26a and miR-30c levels may not drastically affect basal ERK1/2 and p38 MAPK phosphorylation levels. [score:1]
Cells were also co -transfected with the synthetic Snail1 3′-UTR plasmid, control plasmid (β-gal), and miR-26a or miR-30c mimic alone, a combination of miR-26a/30c mimics (each at half the dose for the single mimic treatment) or negative control mimic. [score:1]
Co-treatment with the miR-26a/miR-30c mimic combination showed a trend towards ameliorating ERK1/2 and p38 MAPK phosphorylation, but this effect was not significant. [score:1]
Meanwhile, no repression was observed with the construct containing the Snail1 3′-UTR with a mutated miR-30c binding site (Fig. 2B). [score:1]
Taken together, these results describing the coordination of miR-26a/30c in renal fibrosis provide new insights into the progression of DN, and co-silencing miR-26a and miR-30c could be a novel renoprotective therapy for DN patients. [score:1]
Hence, mimic -induced promotion of miR-26a and miR-30c levels may not drastically affect basal mRNA or protein levels. [score:1]
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2
[+] score: 266
CaMKIIδ has been reported to regulate VSM proliferation through signaling pathways that result in suppression of p53 and p53-targets including CDKN1 (p21), a cell cycle inhibitor 26. miR-30 family members have been reported to function as tumor suppressors by inhibiting cell proliferation, invasion and inducing apoptosis through different mechanisms, such as targeting BCL9 and repressing Wnt signaling 36. [score:14]
Using well-established aortic VSM primary cell culture and vascular injury mo dels, we demonstrated; 1) an inverse correlation between CaMKIIδ protein and miR-30 family expression in VSM cells upon phenotype switching in vitro and in response to vascular injury in vivo; 2) regulation of CaMKIIδ expression and cell proliferation by miR-30 in cultured VSM with magnitude changes comparable to those observed in vivo following vascular injury; and 3) prevention of CaMKIIδ upregulation with inhibition VSM cell proliferation and neointima formation in vivo following ectopic miR-30 expression. [score:13]
Since we demonstrated that miR-30 significantly inhibited VSM proliferation in vitro, in part by targeting CaMKIIδ expression, we tested effects of ectopic miR-30 expression on CaMKIIδ expression and vascular remo deling in vivo following rat carotid artery balloon injury. [score:11]
Overexpression of miR-30 reduces CaMKIIδ expression by targeting CaMKIIδ mRNA 3′UTR and inhibits VSMCs proliferation. [score:9]
In the present studies, miR-30 overexpression decreased CaMKIIδ expression and inhibited VSM proliferation in vitro, an effect that could be partially rescued by re -expression of CaMKIIδ to physiological levels. [score:9]
Based on reciprocal expression dynamics between CaMKIIδ and miR-30 in VSM in vivo in response to vascular injury, we tested the hypothesis that CaMKIIδ is in fact an endogenous target of miR-30 and its expression is regulated by miR-30. [score:8]
Importantly, overexpression of miR-30c significantly inhibited injury -induced CaMKIIδ [2] up-regulation (Fig. 5a). [score:8]
Because the synthetic phenotype cultured VSM cells expressed low levels of miR-30 family members, and effective miR-30 silencing would require siRNAs targeting all of the redundant family members, we relied on gain-of-function approaches to test if CaMKIIδ was, in fact, a direct target for miR-30. [score:8]
Overexpression of miR-30 significantly inhibits CaMKIIδ protein expression in cultured VSMCs. [score:7]
Based on these reports, the current studies, and one report that identified miR-30b as a regulator of CaMKIIδ expression in cardiomyocytes, it is reasonable to propose that dysregulation of a miR-30/CaMKIIδ axis in both VSM and heart might contribute to diverse cardiovascular diseases. [score:7]
CaMKIIδ [2] is involved in miR-30 mediated attenuation of VSM cell proliferationBecause miRs typically have multiple mRNA targets we determined to what extent CaMKIIδ protein expression could rescue miR-30e induced inhibition of VSM proliferation. [score:7]
Additionally, when Shi et al. induced apoptosis using TGF-β in podocytes, miR-30 expression was observed to be down-regulated in a Smad2 -dependent manner 48. [score:6]
Previous studies have suggested coordinate down-regulation of miR-30 family members in skeletal muscle as a function of de-differentiation or dystrophic disease 41, in cardiac muscle as a function of hypertrophy heart failure 42 or atrial fibrillation 43, in human thoracic aortic dissection 44, and in cardiac and VSM cells following ER stress 45 46. [score:6]
Importantly, lentiviral transduction of miR-30 in vivo, immediately following injury, largely prevented subsequent CaMKIIδ upregulation and strongly inhibited VSM cell proliferation and neointimal remo deling. [score:6]
MiR-30 inhibits CaMKIIδ expression by targeting CaMKIIδ 3′UTR in primarily cultured smooth muscle cells. [score:6]
Overexpression of miR-30c dramatically inhibits neointima formation. [score:5]
These experiments confirm CaMKIIδ as a target of miR-30 and mediator of miR-30 induced inhibition of cell proliferation. [score:5]
In primarily cultured rat VSM cells, CaMKIIδ [2] expression was inhibited approximately 50% after introduction of miR-30c or miR-30e mimics introduced by electroporation (Fig. 2b). [score:5]
MiR-30 family member expression is significantly decreased following balloon angioplasty injury of rat carotid arteries coincident with CaMKIIδ upregulation and neointimal vascular remo deling. [score:5]
miR-30c and miR-30e mimics significantly reduced CaMKIIδ protein expression by about 50% and inhibited activity of a luciferase-CaMKIIδ 3′-UTR construct by 30%. [score:5]
Similarly, comparing miR-30 expression in differentiated VSM from intact aorta medial layers to synthetic phenotype cultured aortic medial VSM cells confirmed reduced expression of miR-30a-e in de-differentiated cells by 30–70%. [score:5]
Partial rescue suggests there are other targets of miR-30 in addition to CaMKIIδ that could be involved in miR-30 induced inhibition of VSM cell proliferation. [score:5]
Given the diversity of pathways impinging on cell cycle control, multiple signaling pathways may also be regulated in VSM by miR-30 and contribute to its net inhibitory effects on VSM proliferation. [score:4]
Deletion of the putative miR-30 binding sequence in the CaMKIIδ 3′-UTR construct abrogated the effects of miR-30, supporting the hypothesis that CaMKIIδ is a direct target for miR-30 in VSM. [score:4]
Neointima formation is a balance between VSMC proliferation and apotosis, and our data does not exclude the possibility that miR-30 regulates VSMC apoptosis in vivo, thus contributing to its inhibitory effect on the neointima formation. [score:4]
How to cite this article: Liu, Y. F. et al. MicroRNA-30 inhibits neointimal hyperplasia by targeting Ca [2+]/calmodulin -dependent protein kinase IIδ (CaMKIIδ). [score:4]
Next, we employed a luciferase reporter assay to determine if miR-30 directly interacts with CaMKIIδ 3′UTR, and exert its inhibitory regulation. [score:4]
miR-30c, the most abundant miR-30 family member in vivo, was introduced into the medial wall by lenti-viral transduction immediately after carotid injury in order to rescue injury -induced miR-30 downregulation. [score:4]
We expect that miR-30, miR-145 and other miRs act collectively to regulate the VSM phenotype switch which involves changes in expression of hundreds of proteins. [score:4]
Thus, it needs to be studied if miR-30 interferes with the activation or promotes differentiation of vascular progenitor cells, resulting in the inhibition of neointima hyperplasia. [score:3]
Lenti-viral delivery of miR-30 to the injured carotid artery walls dramatically inhibits cell proliferation in the medial walls and neointima hyperplasia. [score:3]
Collectively, in differentiated carotid arteries (Fig. 1) and aorta (Fig. 2) miR-30 family members are expressed at levels comparable to miR-145 which is considered a high abundance microRNA associated with and regulating the differentiated VSM phenotype 23. [score:3]
Furthermore, overexpression of miR-30 impairs cultured VSM cell proliferation, and CaMKIIδ rescue in the presence of miR-30 partially, but significantly recovers VSM cell growth. [score:3]
The expression of miR-30 family members is reduced in dedifferentiated vascular smooth muscle. [score:3]
Quantifying neoinitmal areas as a ratio to medial wall area indicated a greater than 80% decrease in neointima formation following miR-30c overexpression. [score:3]
Collectively, miR-30 family members are expressed at a level comparable to miR-145. [score:3]
Administration of a lentivirus encoding a pre-miR-30c construct dramatically inhibited neointima formation 14 days after injury comparing to control (Fig. 5b, lower panel). [score:3]
GFP protein expression 2 weeks following injury was comparable between control and miR-30c transduced vessels indicating similar lenti-viral infection efficiencies (Fig. 5a). [score:3]
MiRNA mimics were purchased from Invitrogen and lenti-viral plasmid expressing miR-30c was purchased from System Biosciences. [score:3]
All miR-30 members were expressed in uninjured carotid medial VSM with miR-30c being the most abundant (Fig. 1d). [score:3]
Based on in silico analysis of the rat CaMKIIδ 3′UTR sequence (TARGETSCAN), a miR-30 family binding sequence is predicted ([+2036]UGUUUACA [+2043]) (Fig. 1c). [score:3]
In summary, we have shown that elevated CaMKIIδ protein and attenuated miR-30 expression in dedifferentiated/synthetic vascular smooth muscle cells in vitro and in vivo. [score:3]
To study if miR-30 binds to CaMKIIδ 3′UTR, full-length of CaMKIIδ 3′UTR (Accession: NM_012519.2, +1825 to +2300) and truncated CaMKIIδ 3′UTR (+1825 to +2035) without miR-30 binding site ([+2036]UGUUUACA [+2043]) were cloned into pMIR-REPORT™ miRNA Expression Reporter Vector (Invitrogen). [score:3]
Overexpression of miR-30c prevents injury induced increase of CaMKIIδ and attenuates neointima formation. [score:3]
7 days post vascular injury, expression of all miR-30 family members was significantly reduced in medial wall VSM by 60–80%. [score:3]
Mechanisms underlying coordinate regulation of miR-30 family members are not known. [score:2]
Interestingly, miR-30 family members are encoded on 3 different chromosomes in clustered pairs: miR30a and –c2 on human chromosome 6, miR-30b and-d on chromosome 8, and mir30e and –c1 on chromosome 1. A recent report indicates human coordinate regulation of several miR-30 family members by Mef2 in skeletal muscle 47. [score:2]
Vascular injury induces reciprocal regulation of miR-30 family members and CaMKIIδ protein in rat carotid artery. [score:2]
The expressions of miR-30 family members and miR-145 were compared between injured and uninjured carotid arteries and U6 expression was measured and used for normalization. [score:2]
Moreover, it has been reported that miR-30 regulates epithelial to mesenchymal transition (EMT) and mesenchymal to epithelial transition (MET) in various tumor cells 39 40. [score:2]
MiR-30 inhibits vascular smooth muscle cell proliferation. [score:2]
The significance of the latter experiment is two-fold; confirming miR-30 dependent regulation CaMKIIδ in vivo and suggesting the therapeutic potential for miR-30, at least in the context of restenosis. [score:2]
However, miR-30c had no effect on the truncated CaMKIIδ 3′UTR luciferase activity, suggesting miR-30c directly interacts with CaMKIIδ 3′UTR. [score:2]
In the present studies we focused on CaMKIIδ regulation by miR-30 family members which are predicted to bind to a species-conserved sequence in the CaMKIIδ 3′-UTR. [score:2]
CaMKIIδ [2] is involved in miR-30 mediated attenuation of VSM cell proliferation. [score:1]
When the confluency reached 80–90%, the culture media were replaced with DMEM supplemented with 10% serum and cells were transfected with pPACKH1-GAG (3.3 μg), pPACKH1-REV (3.3 μg), pVSV-G (3.3 μg) and lenti-viral plasmid encoding miR-30c or empty lenti-viral vector (2 μg) using TransIT [®]-2020 (Mirus Bio, WI, USA) (36 μl). [score:1]
The reporter constructs were transiently transfected into HEK293 cells along with miR-30c mimic or a miR control. [score:1]
VSM cells (1 × 10 [6]) were harvested and electroporated with either miR-30c/e mimics (0.1 nmol) or miRNA mimic control (0.1 nmole) (Invitrogen) using the Amaxa Nucleofector system (Lonza) and the VSM cell-specific D33 program (Lonza Amaxa). [score:1]
HEK293 cells were grown on 35mm petri dish and transiently transfected with combinations of CaMKIIδ 3′UTR luciferase reporter (2 μg), TK- Renilla (0.1 μg) and miRNA mimic control (0.4 nmole); CaMKIIδ 3′UTR luciferase reporter (2 μg), TK- Renilla (0.1 μg) and miR-30c mimics (0.4 nmole) or trucanted CaMKIIδ 3′UTR luciferase reporter (2 μg), TK- Renilla (0.1 μg) and miR-30c mimics (0.4 nmole) by using lipofectamine2000 (Invitrogen) and incubated for total 72 h prior to cell lysis. [score:1]
These magnitude changes are comparable to those previously observed in A10 cells using miR-145 23 and the partial effects in both studies could be due redundant effects of the miR-30 and miR-145 species. [score:1]
A full-length CaMKIIδ 3′UTR construct and truncated CaMKIIδ 3′UTR construct without the predicted miR-30 seed sequence ([+2036]UGUUUACA [+2043]) were cloned into a luciferase reporter vector (Fig. 2c). [score:1]
All experiments were carried out with VSM cells from passage 3 to 6. To transduce miR-30 into the common carotid artery wells in vivo, we produced lenti-virus encoding miR-30c using HIV -based pPACKH1 packaging system (System Biosciences, CA, USA). [score:1]
Upon vascular injury or culture of the VSM cells, total miR-30 levels decrease by approximately 75%, similar in magnitude to the decrease in miR-145 and coincident with the switch to a VSM cell synthetic phenotype. [score:1]
Rat carotid artery was balloon injured and locally infected with lentivirus encoding GFP and miR-30c. [score:1]
GFP was also encoded by both control and miR-30c lenti-virus. [score:1]
For experiments delivering lenti-virus encoding miR-30c and control lenti-virus to the injured segment of the common carotid artery, prior to the second complete ligation, concentrated lenti-virus media were injected into and incubated in the injured common carotid artery lumen for 30min, followed with removal of virus media from the artery lumen. [score:1]
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3
[+] score: 217
In the presence of the miR-30c inhibitor, we first displayed that there was no difference in apoptosis between treatment with the miR-30c inhibitor only and the negative control inhibitor; however, downregulation of miR-30c with the inhibitor significantly aggravated cisplatin -induced cell apoptosis in HK-2 and NRK-52E cells as shown in Figures 3c and d. These results suggest that miR-30c might be involved in regulating cisplatin -induced cell apoptosis. [score:13]
Finally, upregulation of miR-30c was shown to alleviate the cisplatin -induced high expression levels of Bnip3L and Hspa5, while downregulation of miR-30c aggravated the cisplatin -induced high expression levels of Bnip3L and Hspa5 (Figure 5). [score:11]
To be on the safe side, we determined the expression levels of Adrb1, Bnip3L, Hspa5 and MAP3K12 in HK-2 cells following either downregulation or upregulation of miR-30c (Figure 5). [score:9]
In addition, when miR-30c was downregulated with the miR-30c inhibitor, we distinctly found that the expression of Bnip3L and Hspa5 was elevated. [score:8]
To investigate whether miR-30c is involved in regulating cisplatin -induced apoptosis, we used the transfection of either the miR-30c mimic (upregulation) or miR-30c inhibitor (downregulation) in HK-2 cells and NRK-52E cells (Figure 3). [score:8]
Furthermore, the elevated expression of both Bnip3L and Hspa5 induced by cisplatin exposure was significantly suppressed by overexpression of miR-30c. [score:7]
Interestingly, we discovered that the expression levels of miR-30a, miR-30b, miR-30c, miR-30d and miR-30e were markedly inhibited by cisplatin exposure, especially that of miR-30b, miR-30c and miR-30e as the inhibition was significantly different from that on day 1 of cisplatin injection (Figure 1j). [score:7]
Bnip3L and Hspa5 could be the target genes of miR-30c in cisplatin -induced apoptosis in renal tubular epithelial cellsTo explore the target genes of miR-30c, we used bioinformatics tools, including TargetScan. [score:7]
Furthermore, we also demonstrated that miR-30a-e expression was markedly inhibited in HK-2 (Figure 2g) and NRK-52E (Figure 2h) cells exposed to cisplatin, further confirming the observation in renal tissue in Figure 1. As shown on Figures 1 and 2, miR-30b and miR-30c were expressed stronger than miR-30a, miR-30d and miR-30e in renal tubular cells and tissues. [score:7]
Likewise, we also found that the expression levels of Bnip3L and Hspa5 were elevated by cisplatin exposure in renal tissue (Figure 4c), but not much of a significant change was found in the expression of Adrb1 and MAP3K12, indicating that Bnip3L and Hspa5 were more likely to be the target genes for miR-30c. [score:7]
In the presence of the miR-30c mimic (upregulation), we could see that the miR-30c mimic alone did not affect apoptosis, but upregulation of miR-30c with the mimic significantly decreased the cisplatin -induced elevated apoptosis. [score:7]
As shown in Figure 5a, only the expression levels of Bnip3L and Hspa5 were reduced when miR-30c was upregulated with the miR-30c mimic. [score:6]
By comparing the upregulated genes in the cisplatin -induced kidney injury mo dels, we chose putative genes, including Adrb1, Bnip3L, Hspa5 and MAP3K12, as possible target genes of miR-30 s as they were in the intersection of both database queries (Figure 4a). [score:6]
23, 24 Moreover, we detected the expression of the miR-30 family in renal tissue and found that miR-30c was the highest expressed miRNA among the five members (Figure 1i). [score:5]
To elucidate the target genes of miR-30 in cisplatin -induced cell apoptosis, we used bioinformatics tools to predict potential potent target genes. [score:5]
Further assessment of these four genes (Adrb1, Bnip3L, Hspa5 and MAP3K12) was implemented to determine the effect of cell apoptosis induced by cisplatin in renal tubular epithelial cells and HK-2 cells, and the results indicated that Bnip3L and Hspa5 were more likely the target genes of miR-30c as the expression levels of both genes showed significant alterations in the presence of cisplatin induction (Figures 4b and c). [score:5]
To assess whether or not Bnip3L or Hspa5 contributed proximal tubular cell apoptosis induced by cisplatin, we overexpressed Bnip3L or Hspa5 in HK-2 cells along with miR-30c overexpression and cisplatin treatment. [score:5]
All of mimic negative control, miR-30c mimic, miRNA inhibitor negative control and miR-30c inhibitor were purchased from Ribobio (Guangzhou, China). [score:5]
To explore the target genes of miR-30c, we used bioinformatics tools, including TargetScan. [score:5]
Moreover, the cisplatin -induced elevated expression of Bnip3L and Hspa5 was increased in the miR-30c inhibitor groups (Figure 5b). [score:5]
To further confirm which genes could be the target genes for miR-30c, we determined the expression levels of Adrb1, Bnip3L, Hspa5 and MAP3K12 in renal tubular epithelial cells and HK-2 cells exposed to cisplatin (Figures 4b and c). [score:5]
[38] Guo et al. [38] demonstrated that miR-30e, as a member of the miR-30 family, protected against aldosterone -induced podocyte apoptosis and mitochondrial dysfunction by directly targeting Bnip3L. [score:4]
Although the in vivo evidence about the role of miR-30c on cisplatin -induced renal tubular cell apoptosis lacks, our current experimental results in this study are generally consistent with the observation in which podocyte apoptosis induced by either TGF-beta or puromycin aminonucleoside treatment was ameliorated by exogenously expressing miR-30 and aggravated by the knockdown of miR-30. [score:4]
[25] Furthermore, previous studies demonstrated that the dysregulation of miR-30c would cause several serious kidney diseases such as diabetic nephropathy, [26] renal fibrosis, [27] ischemia-reperfusion -induced kidney injury [28] and contrast -induced AKI. [score:4]
[34] Here we revealed that all of the miR-30 miRNAs, including miR-30a, miR-30b, miR-30c, miR-30d and miR-30e, were downregulated in both renal tubular epithelial cells and HK-2 cells when cell apoptosis in renal tubules was induced by cisplatin exposure (Figures 1 and 2). [score:4]
Manipulating miR-30c expression in HK-2 and NRK-52E cells directly altered the effect of cisplatin -induced cell apoptosis. [score:4]
These results indicate that Bnip3L and Hspa5 genes function as the direct targets of miR-30c during the proximal tubular cell apoptosis caused by cisplatin. [score:4]
Cell apoptosis was attenuated when miR-30c was activated, while miR-30c inhibition caused the aggravation of cell apoptosis (Figure 3). [score:3]
Bnip3L and Hspa5 could be the target genes of miR-30c in cisplatin -induced apoptosis in renal tubular epithelial cells. [score:3]
[36] Roca-Alonso et al. [37] reported that miR-30 overexpression protects cardiac cells from doxorubicin -induced apoptosis. [score:3]
Flow cytometry was used to determine cell apoptosis following the manipulation of miR-30c expression in HK-2 (Figure 3a) and NRK-52E (Figure 3b) cells. [score:3]
All these data further confirm that Bnip3L or Hspa5 serve as the target genes of miR-30c and mediated renal tubular cell apoptosis induced by cisplatin. [score:3]
[30] We preliminarily chose Adrb1, Bnip3L, Hspa5 and MAP3K12 through comparing the elevated genes and the miR-30c target gene prediction (Figure 4a). [score:3]
Manipulating miR-30c expression alters the effect of cisplatin -induced apoptosis in proximal tubule epithelial cells. [score:3]
As shown on Figures 7c and d, Bnip3L or Hspa5 overexpression abolished miR-30c effects on the cisplatin -induced apoptosis. [score:3]
Likewise, we revealed that the expression levels of miR-30b and miR-30c were higher than that of the other three members in HK-2 (Figure 2e) and NRK-52E (Figure 2f) cells. [score:3]
Subsequently, Bnip3L and Hspa5 were confirmed to more likely be the target genes of miR-30c in cisplatin -induced injury of renal tubules. [score:3]
Using bioinformatics tools, we predicted putative genes, including Adrb1, Bnip3L, Hspa5 and MAP3K12, to be the target genes of miR-30. [score:3]
The results from previous studies further confirmed our hypothesis that Bnip3L and Hspa5 are target genes of miR-30c based on our current experimental results. [score:3]
Moreover, the wild-type reporter but not the mutant yielded a higher luciferase activity in miR-30c inhibitor -transfected cells (Figures 6c and d). [score:3]
Then, we further performed luciferase reporter assays using reporters carrying either the wild-type 3′-untranslated region (UTR) of human Bnip3L and Hspa5 or mutant nucleotides swapped in the region corresponding to the miR-30c ‘seed’ (Figures 6a and b). [score:2]
All of these reports and our results reveal that the miR-30 family indeed has a regulatory role in the modulation of the cell cycle and cell apoptosis in a variety of pathophysiological processes. [score:2]
There is no doubt that our current study on miR-30c function may markedly contribute to the goal to minimize cisplatin -induced nephrotoxicity, although the precise molecular biological mechanism and in vivo experimental evidence how miR-30c mediates apoptosis of renal tubular cell must still be addressed in the future. [score:1]
[29] Hence, miR-30c was chosen for the following functional experiments in this study. [score:1]
When HK-2 cells were co -transfected with the synthetic miR-30c mimic, the wild-type reporter exhibited reduced luciferase activity, but the mutant did not. [score:1]
The wild-type 3′-UTR fragment of human Bnip3L and Hspa5 that contained the putative binding site for miR-30c was obtained by PCR. [score:1]
The reason for focusing on this family is that the miR-30 family is the highest abundant miRNA family in renal tubular epithelial cells according to the results of our previous gene microarray. [score:1]
In this study, we focused on the role of the miR-30 family in the protection of renal tubular cells from the injury induced by cisplatin. [score:1]
Furthermore, the cisplatin -induced apoptosis in HK-2 and NRK-52E cells was affected by changes in miR-30c. [score:1]
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r = −0.56, P = 0.0143 To determine whether CTHRC1 is a direct downstream target of miR-30c, we firstly transfected miR-30c mimics or miR-30c inhibitor into BT549 cells, and then detected CTHRC1 expression level with qRT-PCR and western blot. [score:8]
In addition, CTHRC1 promoted cell proliferation, invasion and migration and suppressed cell apoptosis in breast cancer, which might be by activating GSK-3β/β-catenin signaling and inhibiting Bax/Caspase-9/Caspase-3 signaling respectively; and these biological functions of CTHRC1 could be directly negatively regulated by miR-30c. [score:7]
We thus detected Bax with western blot and found ectopic expression of miR-30c markedly increased the expression level of Bax, which could be mimicked by loss of CTHRC1, whereas gain of CTHRC1 decreased Bax expression (Fig. 6b). [score:7]
In this study, we found CTHRC1 promoted cell proliferation, invasion and migration and suppressed cell apoptosis in breast cancer, which might be by activating GSK-3β/β-catenin signaling and inhibiting Bax/Caspase-9/Caspase-3 signaling respectively; and these biological functions of CTHRC1 could be directly negatively regulated by miR-30c. [score:7]
A, The relative expression level of miR-30c overexpression and inhibition in indicated cells was detected by qRT-PCR. [score:7]
Therefore, we suppose strategies designed to up-regulate miR-30c or down-regulate CTHRC1 may provide a promising method to alleviate breast cancer progression. [score:7]
Our data demonstrated that CTHRC1, negatively regulated by miR-30c, promoted cell proliferation, invasion and migration and suppressed cell apoptosis in breast cancer, which might be by activating GSK-3β/β-catenin signaling and inhibiting Bax/Caspase-9/Caspase-3 signaling respectively. [score:6]
showed restoration of miR-30c markedly suppressed the phosphorylation of GSK-3β at Ser9, which could be mimicked by knock-down of CTHRC1, whereas overexpression of CTHRC1 significantly promoted the phosphorylation of GSK-3β (Fig. 6a). [score:6]
d Schematic representation of the major molecular mechanism that miR-30c/CTHRC1 axis exerts its role in cell proliferation, apoptosis, invasion and migration Taken together, the above data indicated CTHRC1, negatively regulated by miR-30c, might promote cell proliferation, invasion and migration by activating GSK-3β/β-catenin signaling and suppress cell apoptosis by inhibiting Bax/Caspase-9/Caspase-3 signaling (Fig. 6d). [score:6]
d Schematic representation of the major molecular mechanism that miR-30c/CTHRC1 axis exerts its role in cell proliferation, apoptosis, invasion and migration Taken together, the above data indicated CTHRC1, negatively regulated by miR-30c, might promote cell proliferation, invasion and migration by activating GSK-3β/β-catenin signaling and suppress cell apoptosis by inhibiting Bax/Caspase-9/Caspase-3 signaling (Fig. 6d). [score:6]
We found miR-30c mimics markedly decreased the luciferase activity of Wt 3′ UTR of CTHRC1, whereas miR-30c inhibitor up-regulated the luciferase activity; and the luciferase activity of Mut 3′ UTR of CTHRC1 showed no significant difference (Fig. 4d). [score:6]
In this study, BT549 and HEK293T cells were transfected with miR-30c mimics, negative control, miR-30c inhibitor and inhibitor negative control. [score:5]
c Correlation analysis of miR-30c expression and CTHRC1 expression in clinical breast cancer samples. [score:5]
Next we cloned wild-type and mutant CTHRC1–3′ UTR target sequences into the luciferase reporter vector (Fig. 4c) and transfected into HEK293T cells with miR-30c mimics or inhibitor also transfected. [score:5]
In addition, Rodr et al. [18] and Bockhorn et al. [19] have successively reported the low expression of miR-30c was associated to poor prognosis in breast cancer, whereas our data showed CTHRC1 high -expression indicated poor prognosis. [score:5]
Transwell invasion/migration assay demonstrated restoration of miR-30c markedly suppressed invasion and migration of BT549 cells, which could be mimicked by knock-down of CTHRC1, whereas overexpression of CTHRC1 significantly increased cell invasion and migration (Fig. 5e). [score:5]
Western analyses showed that the caspase-9 and caspase-3 were significantly elevated after restoration of miR-30c, which was mimicked in the group with CTHRC1 knock-down, whereas gain of CTHRC1 markedly down-regulated caspase-9 and caspase-3 (Fig. 6b). [score:5]
Moreover, our previous miRNA microarray analysis also revealed that miR-30c was significantly down-regulated in breast cancer tissues (Additional file 4: Figure S2B). [score:4]
CTHRC1 is a direct target of miR-30c. [score:4]
Therefore, these data indicated CTHRC1, which was negatively regulated by miR-30c, promoted cell proliferation, invasion and migration, and inhibited cell apoptosis. [score:4]
In the present study, we demonstrated that CTHRC1, negatively regulated by miR-30c, could promote breast cancer cell proliferation, invasion and migration and suppress cell apoptosis. [score:4]
Fig. 4CTHRC1 is a direct target of miR-30c. [score:4]
We supposed those breast cancer patients with CTHRC1 high -expression could be characterized into poor prognosis group, whose therapeutic effect of traditional strategies was not so good, and might be treated with strategies designed to up-regulate miR-30c. [score:4]
showed gain of miR-30c decreased both mRNA and protein level of CTHRC1, and loss of miR-30c caused up-regulation of CTHRC1 (Fig. 4a, b). [score:4]
Thus, these data indicated that loss of miR-30c was related to the up-regulation of CTHRC1. [score:4]
B, miRNA microarray analysis revealed miR-30c was significantly down-regulated in breast cancer tissues. [score:4]
Compared with matched PBC, miR-30c in BC was frequently down-regulated (Fig. 3b). [score:3]
Fig. 3CTHRC1 and miR-30c expression are inversely correlated in human breast cancer cells and tissues. [score:3]
Flow cytometry revealed that ectopic expression of miR-30c markedly increased cell apoptosis rate, which could be mimicked by loss of CTHRC1, whereas gain of CTHRC1 decreased apoptosis rate (Fig. 5d). [score:3]
We further adopted colony formation assay and found restoration of miR-30c markedly decreased the number of colonies, which could be mimicked by knock-down of CTHRC1, whereas overexpression of CTHRC1 significantly increased the number of colonies (Fig. 5b). [score:3]
We firstly detected β-catenin and its active (dephosphorylated) form with western blot, and found ectopic expression of miR-30c resulted in a markedly decrease of β-catenin and its active form, which could be mimicked by loss of CTHRC1 with CTHRC1-siRNA, whereas gain of CTHRC1 significantly increased β-catenin and its active form (Fig. 6a). [score:3]
We detected miR-30c in normal breast tissue, 5 benign breast tumor tissues and 18 paired breast cancer tissues with qRT-PCR, and results were normalized with its expression in normal tissue. [score:3]
Therefore, we hypothesized miR-30c/CTHRC1 axis might also exert its role by targeting GSK-3β/β-catenin signaling in breast cancer. [score:3]
Fig. 5Ectopic expression of miR-30c or gain and loss of CTHRC1 affects breast cancer cell proliferation, apoptosis, invasion and migration. [score:3]
Fig. 6Ectopic expression of miR-30c or gain and loss of CTHRC1 affects GSK-3β/β-catenin signaling and Bax/Caspase-9/Caspase-3 signaling in breast cancer. [score:3]
Furthermore, there was an inverse correlation between the expression of miR-30c and CTHRC1 in breast cancer tissues (Fig. 3c, r = −0.56, P = 0.0143). [score:3]
demonstrated ectopic expression of miR-30c resulted in a markedly decreased cell viability, which could be mimicked by loss of CTHRC1 with CTHRC1-siRNA, whereas gain of CTHRC1 significantly increased cell viability (Fig. 5a). [score:3]
a The relative expression level of miR-134, miR-155, miR-30c and miR-630 in breast cancer cells respectively was detected by qRT-PCR. [score:3]
CTHRC1 and miR-30c expression are inversely correlated in human breast cancer cells and tissues. [score:3]
The relative expression level of miR-134, miR-155, miR-30c and miR-630 in breast cancer cells respectively was detected by qRT-PCR. [score:3]
Taken together, these results demonstrated that CTHRC1 was directly regulated by miR-30c. [score:3]
Then we investigated the expression of these candidate miRNAs in nontumorigenic breast epithelial cell line MCF-10A and breast cancer cells by qRT-PCR and found only miR-30c was markedly down-regulated in breast cancer cells compared to MCF-10A (Fig. 3a). [score:3]
Ectopic expression of miR-30c or gain and loss of CTHRC1 affects GSK-3β/β-catenin signaling and Bax/Caspase-9/Caspase-3 signaling in breast cancer. [score:3]
Ectopic expression of miR-30c or gain and loss of CTHRC1 affects breast cancer cell proliferation, apoptosis, invasion and migration. [score:3]
Taken together, we identified the role of miR-30c/CTHRC1 axis in breast cancer progression and demonstrated CTHRC1 may serve as a prognostic biomarker and therapeutic target for breast cancer. [score:3]
demonstrated the β-catenin in nucleus was decreased evidently after ectopic expression of miR-30c, which was mimicked by loss of CTHRC1, whereas gain of CTHRC1 enhanced the nuclear localization of β-catenin (Fig. 6c). [score:3]
Also, cell cycle analysis revealed a significant increase in the percentage of cells in G1 phase and a decrease in the percentage of cells in S phase in cells transfected with miR-30c, which could be mimicked by CTHRC1 knock-down, whereas gain of CTHRC1 decreased the proportion of cells in G1 phase and increased the proportion of cells in S phase (Fig. 5c). [score:2]
a The effect of ectopic expression of miR-30c or gain and loss of CTHRC1 on cell viability was detected by CCK-8 assay. [score:2]
All of these further prompted us to postulate miR-30c was potential critical upstream negative regulator of CTHRC1. [score:2]
To confirm the interference efficiency on miR-30c and CTHRC1. [score:1]
Therefore, we focused on miR-30c for further study. [score:1]
Next we explored the role of miR-30c/CTHRC1 axis in cell apoptosis. [score:1]
We used miRwalk database to identify potential miRNAs that bind to 3′ UTR of CTHRC1 and identified miR-134, miR-155, miR-30c and miR-630 as possible candidates (Additional file 4: Figure S2A). [score:1]
Breast cancer Prognosis Metastasis CTHRC1 miR-30c Breast cancer is the most frequently diagnosed cancer and the leading cause of cancer death among females worldwide [1]. [score:1]
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orting results showed that H2S pretreatment also downregulated miR-30c expression and upregulated Beclin-1 and LC3II expression in spinal cord. [score:11]
The underlying mechanism is that administration of H2S activates autophagy that indicated by upregulation the expression of autophagy-related proteins including Beclin-1 and LC3II via inhibiting miR-30c expression after spinal cord reperfusion injury. [score:10]
Because the mature sequences are highly conserved between miR-30c and miR-30a, and miR-30a was discovered to act as a negative regulator of autophagy through altering the expression of the key autophagy-promoting gene Beclin-1 [22], we thus tested whether miR-30c could also target Beclin-1 expression. [score:8]
To confirm this cellular metabolism, hippocampal neurons was transfected with pre-miR-30c or anti-30c to examined expression of Beclin-1. The data indicated the negative regulation of miRNA or protein expression of Beclin-1 by miR-30c. [score:6]
In vitro, miR-30c was showed to exert negative effect on Beclin-1 expression by targeting its 3’UTR in SY-SH-5Y cells treated with Oxygen, Glucose Deprivation (OGD). [score:5]
ischemic negative control group To further demonstrate the effect of miR-30c on Beclin-1 expression, we transfected SY-SH-5Y cells with pre-miR-30c, anti-30c or their negative control, and then examined the expression of Beclin-1 in cells treated with OGD. [score:5]
was performed to examined levels of miR-30c expression and the results showed declined expression of miR-30c in cells treated with NaSH (Fig.   3b) which is consistent to that in spinal cord. [score:5]
ischemic negative control groupTo further demonstrate the effect of miR-30c on Beclin-1 expression, we transfected SY-SH-5Y cells with pre-miR-30c, anti-30c or their negative control, and then examined the expression of Beclin-1 in cells treated with OGD. [score:5]
Additionally, we attempted to detected the possible regulated LC3 by miR-30c and the result showed that the LC3 expression varied as Beclin-1 (Fig.   4d) indicating the key regulated role of miR-30c in OGD -induced cells autophagy. [score:5]
In addition, we confirmed and are the first to note that the miR-30c was downregulated during spinal cord protective effect of H2S in I/R injury. [score:4]
Consistently, in our study of the roles of miR-30 in regulation of autophagy, we observed that only expression of miR-30c showing around 62 % decrease during activation of autophagy under I/R injury conditions in Fig.   2a. [score:4]
miR-30c acts as a negative regulator of Beclin-1 expression. [score:4]
miR-30c is predicted to have the a consensus sequences within the 3’UTR of Beclin-1 (Fig.   4a), we took advantage of the Beclin-1 dual luciferase reporter system to study the role of miR-30c in regulation of Beclin-1 expression. [score:4]
The result showed no changes in expression of miR-30 except that decreased in miR-30c (Fig.   2a) suggesting an involvement of miR-30c in neuroprotective effect against spinal cord ischemia-reperfusion injury of H2S. [score:3]
I/R group To explore the mechanisms how H [2]S could attenuate I/R -induced spinal cord injury, we examined the expression of miR-30 profiles by using. [score:3]
Fig. 4Targeting site of miR-30c in the Beclin-1 3’UTR. [score:3]
cells treated without NaHS Spinal core protective effect of H [2]S was reversed by miR-30c overexpressionExperiments in SY-SH-5Y cells demonstrated that miR-30c played an important role in H2S -induced autophagy after OGD injury. [score:3]
In rat mo del of I/R injury, pretreatment of pre-miR-30c or 3-MA (an inhibitor for autophagy) can abrogated spinal cord protective effect of H2S. [score:3]
The mimics and inhibitors of hsa-miR-30c and their negative controls (RIBO Bio, Guangzhou, P. R. China) were cotransfected with the reporter plasmids at a final concentration of 100 nmol/μl. [score:3]
Recent study showed that miR-30 could impair autophagic process by targeting multiple genes in the autophagy pathway [27]. [score:3]
S [2]H inhibited Beclin-1 3’UTR under OGDTo ascertain the role of miR-30c in protective effect of H2S in autophagy, cells were pretreated NaSH at dose of 10, 100 and 200 μmol/L before OGD treatment and Beclin-1 3’UTR activity was examined. [score:3]
Although no evidence for miR-30c in spinal cord I/R injury, it has been proved to be a neural protector by targeting brain derived neurotrophic factoras well as neurotrophin signaling and axon guidance [10]. [score:3]
To assess the effect of miR-30c on the activation of cells autophagy in ischemic spinal cord, BBB scores and infarct zone were detected after reperfusion in rat spinal cord injected with pre-miR-30c or 3-MA, an inhibitor for antophagy. [score:3]
Based on bioinformatics analysis, we predicted that hsa-miR-30c can bind with the 3’UTR region of Beclin-1 by using four common websites (Target Scan: http://www. [score:3]
Spinal core protective effect of H [2]S was reversed by miR-30c overexpression. [score:3]
OGD group Recent study showed that miR-30 could impair autophagic process by targeting multiple genes in the autophagy pathway [22]. [score:3]
Thus, we hypothesized that there exists the possible targeting region of Beclin-1 mRNA by miR-30c, and it was supported by the result of bioinformatics analysis in Fig.   4a. [score:3]
Cell treatment with miR-30c inhibitor or mimics. [score:3]
For Beclin-1 3’UTR reporter assay, SY-SH-5Y cells were placed in 24-well plates (1 × 10 [3] cells per well) and then transfected with either psi-CHECKTM2-WT-BECN-3’UTR (wild type) or psi- CHECKTM2-MT-BECN-3’UTR that containing the miR-30c targeting sequence (UGUUUAC) (mutant) dual Luciferase reporter plasmid (Promega, WI, USA) according to manufacture’s protocol. [score:2]
Fig. 2Expression of microRNA30 profiles and autophagy-related protein in rats spinal cord. [score:2]
H2S protects spinal cord and induces autophagy via miR-30c in a rat mo del of spinal cord hemia-reperfusion injury. [score:1]
Nevertheless, the precise mechanism by which miR-30c affects autophagic process remains unclear. [score:1]
Based on miRNA being involved in H2S protected against ischemic injury [11], we speculates that miR-30c might be involved in H2S protecting I/R injury. [score:1]
Rats were pretreated with pre-miR-30c (injected in injury site of the spinal cord 24 h before reperfusion, 100 nmol/l) or 3-MA (intraperitoneally injected, 15 mg/kg) before reperfusion. [score:1]
To ascertain the role of miR-30c in protective effect of H2S in autophagy, cells were pretreated NaSH at dose of 10, 100 and 200 μmol/L before OGD treatment and Beclin-1 3’UTR activity was examined. [score:1]
SY-SH-5Y cells were treated with pre-miR-30c or anti-30c (Ambion Pre-miR miRNA Precursors, Life Technologies) using Oligofectamine (Life Technologies) according to the manufacturer’s instructions. [score:1]
Fig. 6Protective effect of H [2]S on I/R injury was reversed by miR-30c in rats. [score:1]
H2S may serve as a neuroprotectant to treat I/R -induced spinal cord injury via activating autophagy in a miR-30c dependent signaling pathway. [score:1]
Autophagy Beclin-1 miR-30c Microtubule associated protein 1 light chain 3 (LC3) Oxygen glucose deprivation (OGD) Ischemia/reperfusion (I/R) injury of the spinal cord is a dynamic process that frequently occurs during a variety of clinical situations such as thoracoabdominal aortic surgery or spinal cord injury [1]. [score:1]
The highly conserved mature miR-30c sequence and potential binding between the miR-30c seed region to the mouse Beclin-1 3’UTR sequence are shown. [score:1]
As shown in Fig.   4b, co-transfection of the SY-SH-5Y cells with a pre-miR-30c (100 nM) led to a significant reduction of the reporter gene activity, in comparison with the cotransfection with a control miRNA. [score:1]
Additionally, quantitative analysis of spinal cord infarction zone showed that H2S induced-alleviation of I/R spinal cord injury was also obviously abrogated by spinal cord treated with pre-miR-30c or 3-MA (Fig.   6b). [score:1]
cells treated without NaHS Experiments in SY-SH-5Y cells demonstrated that miR-30c played an important role in H2S -induced autophagy after OGD injury. [score:1]
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For miR-30c-5p, 25 target genes were down-regulated and 10 target genes were up-regulated at 4 weeks in the MI group compared with the control group. [score:10]
With the exception of miR-143-3p, we observed that changes in the expression of miR-30a-5p, miR-30c-5p, miR-145-5p, and miR-140-3p at 4 weeks post-MI tended to increase compared to the control group, whereas expression of these four miRNAs decreased and the expression of miR-143-3p increased in the SkM treatment group, suggesting that these miRNAs could be associated with the SkM therapy of myocardial injury. [score:6]
Interestingly, as shown in Fig.   3, at 4 weeks post-MI, with the exception of miR-143-3p, changes in miR-30a-5p, miR-30c-5p, miR-145-5p, and miR-140-3p expression tended to increase compared to the control group, whereas the expression of these four miRNAs decreased and the expression of miR-143-3p increased in the SkM +MI group, suggesting that these miRNAs may be associated with SkM therapy in myocardial injury. [score:6]
We focused on changes in some apoptosis -associated miRNA and in gene expression in response to SkM MI therapy, corroborated some of the results obtained from microarrays with real-time qPCR analysis, and selected some significant miRNAs, including miR-30a-5p, miR-30c-5p, miR-145-5p, miR-143-3p, and miR-140-3p, which were involved with anti-apoptotic target genes such as Angptl4, Dpep1, Egr1, Eif5a, Tsc22d3, Irs2 and Cebpb. [score:5]
We observed a significant trend in the expression of some apoptosis-related miRNA and mRNA, including the expression of miR-30a-5p, miR-30c-5p, miR-145-5p, miR-143-3p, and miR-140-3p (Fig.   3). [score:5]
GO-Analysis based on miRNA targeted genes showed significant function of target genes by rno-miR-30a-5p, rno-miR-30c-5p, rno-miR-140-3p, rno-miR-143-3p, and rno-miR-145-5p. [score:5]
Pathway analysis based on miRNA targeted genes showed significant pathways targeted by rno-miR-30a-5p, rno-miR-30c-5p, rno-miR-140-3p, rno-miR-143-3p, and rno-miR-145-5p. [score:5]
We focused on a novel set of apoptosis -associated miRNAs and their target genes, among which 4 miRNAs (miR-30a-5p, miR-30c-5p, miR-145-5p, miR-140-3p), except one (miR-143-3p), were downregulated in the SkM treated group as compared to the untreated group. [score:5]
MicroRNA-GO-Network, screening out the main function of the target genes regulated by rno-miR-30a-5p, rno-miR-30c-5p, rno-miR-140-3p, rno-miR-143-3p, and rno-miR-145-5p. [score:4]
We here confirm that miR-30a-5p and miR-30c-5p might target genes participating in the regulation of apoptosis. [score:4]
We observed that, together, miR-30a-5p and miR-30c-5p might target genes involved in the regulation of apoptosis in MI treated with SkMs. [score:4]
Our data also suggest that some apoptosis -associated miRNAs, such as miR-30a-5p, miR-30c-5p, miR-145-5p, miR-143-3p, miR-140-3p and their target genes, may play an important role in myocardial injury after MI. [score:3]
MIRANDA, MICROCOSM, and MIRDB programs were employed to predict potential targets of five key miRNAs, miR-30a-5p, miR-30c-5p, miR-145-5p, miR-143-3p, and miR-140-3p. [score:3]
Venn’s diagram for target genes of rno-miR-30a-5p, rno-miR-30c-5p, rno-miR-140-3p, rno-miR-143-3p, and rno-miR-145-5p predicted by MIRANDA, MICROCOSM, MIRDB. [score:3]
Moreover, most targeted genes were cooperated on by miR-30a-5p and miR-30c-5p. [score:3]
In this experiment, we focused on a subset of apoptosis-related miRNAs, including miR-30a-5p, miR-30c-5p, miR-145-5p, miR-143-3p, and miR-140-3p, and mRNAs involved in anti-apoptotic target genes such as Angptl4, Dpep1, Egr1, Eif5a, Tsc22d3, Irs2 and Cebpb. [score:3]
We focused on five apoptosis-related miRNAs (miR-30a-5p, miR-30c-5p, miR-145-5p, miR-143-3p, and miR-140-3p), demonstrated their changes after SkMs treatment and filtered out 7 anti-apoptotic target genes, namely, Angpt14, Eif5a, Egr1, Irs2, Cebpb, Tsc22d3, and Dpep1, in the heart tissues (Fig.   6). [score:3]
The five key miRNAs in the network were identified as miR-30a-5p, miR-30c-5p, miR-145-5p, miR-143-3p, and miR-140-3p. [score:1]
The results from real-time qPCR analysis showed high concordance with our microarray results for all investigated transcripts, as shown in Fig.   4. Fig.  4 Analyses of the expression of rno-miR-30a-5p, rno-miR-30c-5p, rno-miR-140-3p, rno-miR-143-3p, and rno-miR-145-5p by RT-PCR. [score:1]
The expression of miR-30a-5p, miR-30c-5p, miR-145-5p, miR-143-3p, and miR-140-3p in the infarcted border zone region was measured by real-time analysis 4 weeks after MI. [score:1]
MiR-30 was shown to induce apoptosis [32] and regulate cell motility by influencing the extracellular matrix remo deling process [33– 35]. [score:1]
The five key miRNAs in the network were identified as miR-30a-5p, miR-30c-5p, miR-145-5p, miR-143-3p, and miR-140-3p, as shown in Additional file 12: Figure S4. [score:1]
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7
[+] score: 78
To do this, we injected the neurone -targeted gene knock-down system (LV-mCMV/SYN-tTA + LV-Tretight-GFP-miR30-shRNA/Luc) with LVV to express Luc in astrocytes (LV-GfaABC [1]D-Luc) and, conversely, the astrocyte -targeted knock-down system (LV-mCMV/GfaABC [1]D-tTA+ LV-Tretight-GFP-miR30-shRNA/Luc) together with LVV for neuronal Luc expression (LV-SYN-Luc). [score:11]
LTR, lentiviral long terminal repeats; Tretight, a modified tetracycline and Dox-responsive promoter derived from pTRE-tight (Clontech); GFP, green fluorescence protein; miR30-shRNA/Luc, miR30 -based shRNA targeting firefly Luc gene; miR30-shRNA/nNOS, miR30 -based shRNA targeting rat neuronal nitric oxide synthase gene; Luc, firefly Luc gene; GfaABC [1]D, a compact glial fibrillary acidic protein promoter (690 bp); SYN, human synapsin 1 promoter (470 bp); mCMV, minimal CMV core promoter (65 bp); GAL4BDp65, a chimeric transactivator consisting of a part of the transactivation domain of the murine NF-κBp65 protein fused to the DNA binding domain of GAL4 protein from yeast; WPRE, woodchuck hepatitis post-transcriptional regulatory element. [score:6]
To this end, we constructed a binary Dox-controllable and cell-specific miR30 -based RNAi system to express shRNAs targeting a reporter gene for Luc and an endogenous gene for nNOS. [score:5]
a: LV-mCMV/GfaABC [1]D-tTA controlled miR30-shRNA/Luc didn't knockdown Luc expression in neurones. [score:4]
b: LV-mCMV/SYN-tTA controlled miR30-shRNA/Luc didn't knockdown Luc expression in glia. [score:4]
These results demonstrate that bidirectional transcriptionally amplified SYN and GfaABC [1]D promoters provide a sufficient level of tTA to activate the Tretight promoter which then drives the synthesis of GFP-miR30-shRNA/Luc transcript to induce substantial Luc knock-down. [score:3]
tTA binds to Tretight promoter in LV-Tretight-GFP-miR30-shRNA/Luc and activates the expression of shRNA/Luc. [score:3]
In these constructs gene targeting sequences were embedded in the precursor miRNA context derived from miR30, one of the most well-studied miRNA in mammals. [score:3]
Abbreviation Vector combination Function LVVs-miRLuc-neuroneLV-SYN-Luc+ LV-Tretight-GFP-miR30-shRNA/Luc+ LV-mCMV/SYN-tTA Neurone-specific Luc knock-down system. [score:2]
LVVs-miRnNOS-neuroneLV-Tretight-GFP-miR30-shRNA/nNOS+ LV-mCMV/SYN-tTA Neurone-specific nNOS knock-down system. [score:2]
LVVs-miRLuc-control2LV-GfaABC [1]D-Luc+ LV-Tretight-GFP-miR30-shRNA/Luc + LV-GfaABC1D-WPRE Control combination used in Luc knock-down experiments for the astrocyte-specific system. [score:2]
LVVs-miRnNOS -negative control1LV-Tretight-GFP-miR30-shRNA/Luc+ LV-mCMV/SYN-tTA Negative control combination used in nNOS knock-down experiments for the neurone-specific system. [score:2]
Again, the anti-Luc construct LV-Tretight-GFP-miR30-shRNA/Luc (treatments 4 in Figure 4c and Figure 4d) did not trigger nNOS knock-down. [score:2]
LVVs-miRnNOS-control2LV-Tretight-GFP-miR30-shRNA/nNOS + LV-GfaABC [1]D-WPRE Control combination used in nNOS knockdown experiments for the astrocyte-specific system. [score:2]
LVVs-miRLuc-gliaLV-GfaABC [1]D-Luc+LV-Tretight-GFP-miR30-shRNA/Luc+LV-mCMV/GfaABC1D-tTA Astrocyte-specific Luc knock-down system. [score:2]
LVVs-miRnNOS-control1 LV-Tretight-GFP-miR30-shRNA/nNOS + LV-SYN-WPRE Control combination used in nNOS knockdown experiments for the neurone-specific system. [score:2]
LVVs-miRnNOS-glia LV-Tretight-GFP-miR30-shRNA/nNOS + LV-mCMV/GfaABC1D-tTA Astrocyte-specific Luc knock-down system. [score:2]
Lentiviral systems developed in the course of this study enable tight Dox-controllable and cell-specific miR30 -based RNAi gene knock-down. [score:2]
LVVs-miRLuc-control1LV-SYN-Luc+ LV-Tretight-GFP-miR30-shRNA/Luc+ LV-SYN-WPRE Control combination used in Luc knock-down experiments for the neurone-specific system. [score:2]
LVVs-miRnNOS -negative control2LV-Tretight-GFP-miR30-shRNA/Luc+ LV-mCMV/GfaABC1D-tTA Negative control combination used in nNOS knock-down experiments for the astrocyte-specific system. [score:2]
It is important to note that anti-Luc construct, LV-Tretight-GFP-miR30-shRNA/Luc (treatment 4 in Figure 4a and Figure 4b), was without effect in either cell line, indicating that the nNOS knock-down was sequence-specific. [score:2]
Figure 3Analyses of the efficacy of miR30-shRNA/Luc in vivo in adult rat brain. [score:1]
First, the effect of miR30-shRNA/Luc was assessed in cell lines. [score:1]
To examine whether the different RNAi efficiency in DVC and HIP is caused by different processing of RNAi, we performed northern blotting analysis to assess the ratio between mature -RNAi and precursor-miR30 -RNAi in these two regions. [score:1]
Analysis of the effects of miR30-shRNA/Luc in vivo. [score:1]
We first confirmed the efficacy of the anti-nNOS construct, LV-Tretight-GFP-miR30-shRNA/nNOS in PC12 and 1321N1 cells. [score:1]
Figure 4Western-blot analyses of the functions of miR30-shRNA/nNOS both in vitro (a, b) and in vivo (c, d). [score:1]
A: LVVs-miRLuc-control1; B: LV-SYN-Luc + LV-Tretight-GFP-miR30-shRNA/Luc + LV-mCMV/GfaABC [1]D-tTA. [score:1]
To construct the LV-Tretight-GFP-miR30-shRNA/nNOS shuttle vector, we replaced the Luc shRNA sequence in the LV-Tretight-GFP-miR30-shRNA/Luc shuttle vector with the nNOS shRNA. [score:1]
Figure 2Analyses of the functions of miR30-shRNA/Luc in vitro. [score:1]
A': LVVs-miRLuc-control2; B': LV-GfaABC [1]D-Luc + LV-Tretight-GFP-miR30-shRNA/Luc + LV-mCMV/SYN-tTA. [score:1]
To generate the LV-Tretight-GFP-miR30-shRNA/Luc shuttle vector, we excised the Tretight fragment containing the modified Tet-responsive promoter from pTRE-Tight-DsRed2 (Clontech) and inserted it into the pTYF-SW Linker and cloned, into the obtained vector, PCR product of GFP-miR30-shRNA/Luc cassette from pPRIME-CMV-GFP-FF3 (kindly provided by F. Stegmeier, Harvard Medical School) downstream of Tretight promoter. [score:1]
Our constructs, following the design of Stegmeir et al. used flanking and loop sequences from an endogenous miR30 [37]. [score:1]
Analyses of the functions of miR30-shRNA/Luc in vitro. [score:1]
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[+] score: 66
Other miRNAs from this paper: rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2
Our experiments revealed that expression of the miR-30 family was down-regulated in cardiomyocytes of rats from the TAAC group, and that miR-30a expression decreased in hypertrophic cardiomyocytes that had been treated with Ang II. [score:8]
Up-regulation of Autophagy and Down-regulation of miR-30 in Rats with TAAC-Induced Cardiac Hypertrophy. [score:7]
The results of our study indicate that Ang II excessively up-regulates cardiomyocyte autophagy by decreasing miR-30 expression, and that this excessive autophagy promotes the development of myocardial hypertrophy. [score:7]
Taken together, these results provide strong evidence that autophagy mediates the development of myocardial hypertrophy in cardiomyocytes: a down-regulation of miR-30 induced by Ang II leads to excessive autophagy in cardiomyocytes, thereby promoting myocardial hypertrophy. [score:5]
A study by Duisters et al. [10] found that miR-30 family members were significantly down-regulated in mouse hypertrophic hearts and in cardiac biopsies from patients with LVH. [score:4]
The miR-30 family is associated with the development of tumors and other diseases (of the nervous, genital, circulatory, alimentary, and respiratory systems), as well as adipogenesis, cellular senescence, drug metabolism and cell differentiation [16]– [31]. [score:4]
Bioinformatics software predicts that miR-30a may regulate the expression of beclin-1. The function of the miR-30 family is similar to that of other microRNAs. [score:4]
Down-regulation of miR-30 leads to myocardial hypertrophy. [score:4]
The pro-fibrotic protein, connective tissue growth factor (CTGF), was down-regulated by miR-30c, such that structural changes in the extracellular matrix of the myocardium were controlled by miR-30c. [score:4]
Consistent with this, the expression level of miR-30 in the plasma of peripheral blood was elevated in patients with left ventricular hypertrophy (LVH). [score:3]
Autophagy and miR-30 expression in rats after TAAC surgery. [score:3]
circulating miR-30 expression in rats from the TAAC group. [score:3]
The expression of miR-30a, miR-30b and miR-30c was significantly lower in rats from the TAAC group, compared with those in the Sham group (Figure 3D). [score:2]
It was thus of interest to investigate whether the down-regulation of miR-30 might mediate Ang II -induced myocardial hypertrophy. [score:2]
miR-30-regulated Autophagy in Cardiomyocytes. [score:2]
Relationship between the circulating miR-30 level and ventricular wall thickness. [score:1]
Downre-gulation of miR-30 Leads to Myocardial Hypertrophy. [score:1]
Use of plasma miR-30 levels for the diagnosis of LVH reached statistical significance (P = 0.039, Figure 12B). [score:1]
Circulating Levels of miR-30 Increased in Rats Following TAAC Surgery, and in Patients with LVH. [score:1]
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[+] score: 62
Here we confirmed that Mtdh represents a target of mi-R30s in DN, and that the expression of all five miR-30 family members is downregulated in the glomeruli form streptozotocin -induced diabetic rats and HG -induced MPC5 cells. [score:8]
Mtdh protein expression was shown to be increased as well after the treatment with the miR-30 inhibitors (Figure 6e), whereas miR-30 mimics significantly reduced Mtdh expression in HG -induced MPC5 cells (Figure 6f). [score:7]
To assess the effects of miR-30s on the expression of Mtdh, we transiently transfected MPC5 cells with miR-30 inhibitors, synthetic miRNA mimics, or their NCs. [score:5]
Furthermore, miR-30 inhibitors significantly increased the expression of Bax and cleaved caspase 3 (Figure 7c). [score:5]
The obtained results demonstrated that miR-30a, -30b, -30c, -30d, and -30e mimics can significantly inhibit the luciferase activity of the wild-type Mtdh 3′-UTR reporter, but not that of the NC, and that this inhibition was reduced when the mutant reporter, with mutated miR-30 -binding site, was used (Figures 5d–h). [score:5]
Transient transfections with siRNAs, Mdth overexpression vector, miR-30 inhibitors, and miR-30 mimics. [score:5]
These cells were transfected with Mtdh siRNA (50 nM; GenePharma, Shanghai, China) or the overexpression (500 ng per well, GenePharma) the mixture of the mimics or inhibitors (RiboBio, Guangzhou, China) of all five miR-30 family members at the final concentrations of 50 nM, using Lipofectamine 2000 (Invitrogen) for 6 h in OPTI-MEM (Gibco BRL), according to the manufacturers' instructions. [score:5]
Mtdh represents a direct target of the members of miR-30 family. [score:4]
Mtdh mRNA level was shown to be significantly increased following the treatment with miR-30 inhibitors (Figure 6c), whereas miR-30s mimics led to a considerable reduction of Mtdh expression induced by HG (Figure 6d), compared with the corresponding NC treatment groups. [score:4]
Therefore, we studied miR-30 expression in the DN glomeruli and HG -induced MPC5 cells. [score:3]
Afterward, OPTI-MEM was replaced with the complete medium containing 1% FBS, and treated with HG for 48 h after the transfection with siRNAs or mimics, whereas the cells treated with miR-30 inhibitors were not treated with HG. [score:3]
MPC5 were transfected with miR-30 inhibitors, mimics, or the respective NCs. [score:3]
analysis demonstrated that the transfection of cells with miR-30 inhibitors significantly increased the percentage of apoptotic cells compared with the NC group (Figure 7a). [score:2]
[44] The 3′-UTR of Mtdh containing putative miR-30 -binding sites was amplified and cloned into PmiR-RB-REPORT dual-luciferase reporter vector (RiboBio). [score:1]
The treatment with miR-30 mimics considerably decreased HG -induced increase in the levels of these proteins (Figure 7d). [score:1]
Conversely, miR-30 mimics considerably reduced the rate of MPC5 apoptosis induced by HG (Figure 7b). [score:1]
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[+] score: 42
The antagomirs designed to inhibit the expression of endogenous miR-30 members and Antagomir Negative Control were obtained from Ribobio. [score:5]
HWJMSC-EVs Deliver and Restore the Expression of miR-30 in Injured Rat Kidney. [score:3]
Mitochondrial Apoptotic Pathways Are Inhibited by EVs-Derived miR-30. [score:3]
Meanwhile, antagomir -treated EVs group revealed lower miR-30 expression as well as the vehicle group (Figure 2(c)). [score:3]
Quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) showed that IRI caused lower expression of miR-30b, miR-30c, and miR-30d (miR-30a and miR-30e did not exist in rat kidney) and EVs treatment entirely reversed the reduction (Figure 2(a)). [score:3]
We demonstrated that hWJMSC-EVs may ameliorate acute renal IRI by inhibition of mitochondrial fission via miR-30. [score:3]
We next explored the miR-30 expression of rat kidney during IRI in vivo. [score:3]
Given that miR-30 has been reported to regulate mitochondrial fission through the DRP1 pathway on cardiomyocytes [20], we hypothesized that human Wharton Jelly MSCs (hWJMSCs) derived EVs may be involved in the modulation of mitochondrial fission via miR-30, thereby protecting kidney from IRI. [score:2]
To understand how hWJMSC-EVs exert effects on mitochondrial fission, we test whether EVs-derived miR-30 family plays a crucial role in regulating mitochondrial fission through DRP1. [score:2]
EVs-Derived miR-30 Members Regulate Mitochondrial Fission through DRP1. [score:2]
To further explore the mechanism of miR-30 reversion, we used specific miR-30 antagomir to treat MSCs. [score:1]
As we expected, miR-30 antagomir mitigated this effect, especially in miR-30b/c/d antagomir cotreated group. [score:1]
The miR-30 family is involved in several cellular processes, including cardiomyocytes exposed to oxidative stress or ischemia injury and apoptosis of type II alveolar epithelial cells [20, 32, 33]. [score:1]
Here we have identified a miR-30-related antiapoptotic pathway involving DRP1 and mitochondria, which may be one of the mechanisms by which hWJMSC-EVs alleviate renal ischemia reperfusion injury. [score:1]
The absence of miR-30 in EVs canceled the miR-30 restoration effects in normal EVs treatment group in vitro. [score:1]
Then, we treated hWJMSCs with miR-30 antagomir. [score:1]
We used at least six rats for each group: (1) sham (n = 6); (2) vehicle (n = 6); (3) EVs (n = 6); (4) EVs + antagomir control (n = 6); (5) EVs + antagomir miR-30b (n = 6); (6) EVs + antagomir miR-30c (n = 6); (7) EVs + antagomir miR-30d (n = 6); (8) EVs + antagomir miR-30b/c/d (n = 6). [score:1]
The sequence of miR-30b antagomir is 5′-AGCUGAGUGUAGGAUGUUUACA-3′; miR-30c antagomir is 5′-GCUGAGAGUGUAGGAUGUUUACA-3′; miR-30d antagomir is 5′-CUUCCAGUCGGGGAUGUUUAGA-3′. [score:1]
The levels of miR-30 family members analyzed by qRT-PCR were normalized to that of U6. [score:1]
Taken together, it appears that EVs-derived miR-30 can block the mitochondrial apoptotic pathways. [score:1]
Our research reveals links among EVs, miR-30, and DRP1 in the apoptotic program of the kidney. [score:1]
Our results suggest that modulation of miR-30 from EVs may represent a therapeutic approach to treat apoptosis-related renal ischemia reperfusion injury. [score:1]
The absence of miR-30 in EVs canceled the miR-30 restoration effects in normal EVs treatment group. [score:1]
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[+] score: 34
miR-30 family was downregulated during pathological hypertrophy to activate calcium signaling, apoptosis and autophagy pathways miR-133b CyclinD, Nelf-A, RhoA, Ccd42 The expression of miR-133 was upregulated during physiological cardiac hypertrophy. [score:9]
It increases cell survival and negatively regulates apoptosis by targeting Bcl2 miR-30 CaMKIIδ, Egfr1, Bcl2 miR-30 was significantly upregulated during physiological hypertrophy. [score:7]
Hence, it is logical to propose that the downregulated expression of miR-30 family in pathological hypertrophy activates calcium signaling, apoptosis and autophagy pathways. [score:6]
angiotensin II induces down-regulation of miR-30 in cardiomyocytes, which in turn promotes myocardial hypertrophy through excessive autophagy [28]. [score:4]
Our data extend these concepts by demonstrating an upregulation of miR-30 family in physiologically hypertrophied rat heart (Fig. 2A, B). [score:4]
Previous studies indicate that angiotensin II induces down-regulation of miR-30 in cardiomyocytes, which in turn promotes myocardial hypertrophy through excessive autophagy [28]. [score:4]
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[+] score: 30
rno-miR-675-5p 4.143757751 Premature senescence of cardiac progenitor cells, G1 arrest, reduced cell proliferation, colony formation, migration and invasion rno-miR-183-3p 3.74730108 Regulates claudin-1 expression rno-miR-299a-5p 3.626723224 Anti-apoptotic role rno-miR-200c-3p 3.593610443 Targets the VEGF-VEGFR2 pathway and angiogenesis rno-miR-665 3.511737089 Negatively targets anti-apoptotic BCL2L1 rno-miR-291a-5p 3.457928187 VSMC migration rno-miR-490-5p 2.373358 Tumour suppressor rno-miR-1 2.505729 Suppresses cell growth rno-miR-133b 2.192279 Inhibits cell proliferation and invasion rno-miR-30c-1-3p 2.70761 Suppresses PXR expression rno-miR-294 2.010496 Promotes proliferation and differentiation rno-miR-127-5p 2.780488 A regulator of MMP-13 and suppresses cell growth rno-miR-503 2.327383 Inhibits cell proliferation and invasion Table 2 Twenty down-regulated miRNAs. [score:26]
Pan et al. reported that miR-30-regulated autophagy mediates angiotensin II -induced myocardial hypertrophy [44], which implies that there exists a complicated network for mediating autophagy that has yet to be determined. [score:2]
It should be noted that the miR-352-IGF2R pathway may not be the only mechanism for regulating autophagy during collateral vessel growth because additional miRNAs involved in autophagy were identified, such as, miR-30. [score:2]
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[+] score: 23
MiR-30 family members are strongly upregulated during adipogenesis in human cells, and inhibition of miR-30 inhibits adipogenesis [12]. [score:8]
In this study, miR-30a, miR-30b, and miR-30c were significantly downregulated in obese mice, and miR-30b was significantly upregulated after LFD feeding. [score:7]
MiR-30c has been found to be upregulated in adipogenesis and to enhance adipogenesis in hASCs, and it appears to target two genes (PAI-1 and ALK2) in distinct pathways [37]. [score:5]
miR-30 family members have also been demonstrated to act as positive regulators of adipocyte differentiation in a human adipose tissue-derived stem cell mo del [35]. [score:2]
The miR-30 family has been found to be important for adipogenesis [12]. [score:1]
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[+] score: 21
The expression of miR-101, miR-30b, miR-30c, miR-30d and miR-27b was detected (Figure 1D) but miR-1 and miR-30e expression was not (data not shown). [score:5]
These results suggested a correlation between the increased expression levels of miR-101, miR-30b, miR-30c, and miR-30d, as well as the decreased Sox9 expression level. [score:5]
However, no negative regulatory effects on Sox9 expression were observed in miR-30b, miR-30c and miR-30d on (Figures 2D and 2E). [score:4]
Six miRNAs (miR-1, miR-101, miR-30b, miR-30c, miR-30d, and miR-30e) were selected to potentially target Sox9 (Figure 1A). [score:3]
The increasing expression of miR-101, miR-30b, miR-30c, and miR-30d emerged at different time points after IL-1β treatment (Figure 1D). [score:3]
However, luciferase activity was not reduced with the mimics of miR-30b, miR-30c, and miR-30d (Figure 2C). [score:1]
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15
[+] 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-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-20a, hsa-mir-22, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-98, hsa-mir-101-1, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-15b, mmu-mir-101a, mmu-mir-126a, mmu-mir-130a, mmu-mir-133a-1, mmu-mir-142a, mmu-mir-181a-2, mmu-mir-194-1, hsa-mir-208a, hsa-mir-30c-2, mmu-mir-122, mmu-mir-143, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-181a-1, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-15b, hsa-mir-122, hsa-mir-130a, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-142, hsa-mir-143, hsa-mir-126, hsa-mir-194-1, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-208a, 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-16-1, mmu-mir-16-2, mmu-mir-18a, mmu-mir-20a, mmu-mir-22, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-29c, mmu-mir-98, mmu-mir-326, rno-mir-326, rno-let-7d, rno-mir-20a, rno-mir-101b, mmu-mir-101b, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-181b-2, mmu-mir-17, mmu-mir-19a, mmu-mir-181a-1, mmu-mir-26a-2, mmu-mir-19b-1, mmu-mir-181b-1, mmu-mir-181c, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-101-2, hsa-mir-26a-2, hsa-mir-378a, mmu-mir-378a, hsa-mir-326, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-181b-2, 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-15b, rno-mir-16, rno-mir-17-1, rno-mir-18a, rno-mir-19b-1, rno-mir-19a, rno-mir-22, rno-mir-26a, rno-mir-26b, rno-mir-29c-1, rno-mir-30c-2, rno-mir-98, rno-mir-101a, rno-mir-122, rno-mir-126a, rno-mir-130a, rno-mir-133a, rno-mir-142, rno-mir-143, rno-mir-181c, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-194-1, rno-mir-194-2, rno-mir-208a, rno-mir-181a-1, hsa-mir-423, hsa-mir-18b, hsa-mir-20b, hsa-mir-451a, mmu-mir-451a, rno-mir-451, ssc-mir-122, ssc-mir-15b, ssc-mir-181b-2, ssc-mir-19a, ssc-mir-20a, ssc-mir-26a, ssc-mir-326, ssc-mir-181c, ssc-let-7c, ssc-let-7f-1, ssc-let-7i, ssc-mir-18a, ssc-mir-29c, ssc-mir-30c-2, hsa-mir-484, hsa-mir-181d, hsa-mir-499a, rno-mir-1, rno-mir-133b, mmu-mir-484, mmu-mir-20b, rno-mir-20b, rno-mir-378a, rno-mir-499, hsa-mir-378d-2, mmu-mir-423, mmu-mir-499, mmu-mir-181d, mmu-mir-18b, mmu-mir-208b, hsa-mir-208b, rno-mir-17-2, rno-mir-181d, rno-mir-423, rno-mir-484, mmu-mir-1b, ssc-mir-15a, ssc-mir-16-2, ssc-mir-16-1, ssc-mir-17, ssc-mir-130a, ssc-mir-101-1, ssc-mir-101-2, ssc-mir-133a-1, ssc-mir-1, ssc-mir-181a-1, ssc-let-7a-1, ssc-let-7e, ssc-let-7g, ssc-mir-378-1, ssc-mir-133b, ssc-mir-499, ssc-mir-143, ssc-mir-423, ssc-mir-181a-2, ssc-mir-181b-1, ssc-mir-181d, ssc-mir-98, ssc-mir-208b, ssc-mir-142, ssc-mir-19b-1, hsa-mir-378b, ssc-mir-22, rno-mir-126b, rno-mir-208b, rno-mir-133c, hsa-mir-378c, ssc-mir-194b, ssc-mir-133a-2, ssc-mir-484, ssc-mir-30c-1, ssc-mir-126, ssc-mir-378-2, ssc-mir-451, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, mmu-mir-378b, mmu-mir-101c, hsa-mir-451b, hsa-mir-499b, ssc-let-7a-2, ssc-mir-18b, hsa-mir-378j, rno-mir-378b, mmu-mir-133c, mmu-let-7j, mmu-mir-378c, mmu-mir-378d, mmu-mir-451b, ssc-let-7d, ssc-let-7f-2, ssc-mir-20b-1, ssc-mir-20b-2, ssc-mir-194a, mmu-let-7k, mmu-mir-126b, mmu-mir-142b, rno-let-7g, rno-mir-15a, ssc-mir-378b, rno-mir-29c-2, rno-mir-1b, ssc-mir-26b
For instance, miR-29c was expressed abundantly in stomach but only in trace amounts in thymus and ovary and miR-30c was relatively strongly expressed in heart, lungs, stomach and endometrium (Figure 3B). [score:5]
miR-22, miR-26b, miR-29c, miR-30c and miR-126 exhibited almost similar expression patterns in all tissues examined (Figure 3B). [score:3]
The observation that miR-22, miR-26b, miR-126, miR-29c and miR-30c are ubiquitously expressed in 14 different tissues of pig is interesting. [score:3]
Additionally, many other miRNAs, such as let-7, miR-98, miR-16, miR22, miR-26b, miR-29c, miR-30c and miR126, were also expressed abundantly in thymus (Figure 3). [score:3]
miR-22, miR-26b, miR-29c and miR-30c showed ubiquitous expression in diverse tissues. [score:3]
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16
[+] score: 11
Another recent study suggested that down-regulation of miR-30 family leads to endoplasmic reticulum stress in vascular smooth muscle cells [25] and a similar trend of down-regulation is shown in the case of miR-30d and miR-30e. [score:7]
Previous studies have shown that miR-30 family members negatively regulate osteoblast differentiation [24] and also suggest RUNX2 and SMAD1 are common post-transcriptional targets of miR-30 family. [score:4]
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17
[+] score: 11
In the mo del group, 17 miRNAs were downregulated, including miR-1, miR-133, miR-29, miR-126, miR-212, miR-499, miR-322, miR-378, and miR-30 family members, whereas the other 18 miRNAs were upregulated, including miR-21, miR-195, miR-155, miR-320, miR-125, miR-199, miR-214, miR-324, and miR-140 family members. [score:7]
Among these differentially expressed miRNAs, miR-1, miR-133, miR-29, miR-126, miR-499, miR-30, miR-21, miR-195, miR-155, miR-199, miR-214, and miR-140 have been reported to be related to MI [25– 36], while the other miRNAs have not been reported directly in MI. [score:4]
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18
[+] score: 11
MiR-107, miR-30 and miR-137 were upregulated only in astrocytes. [score:4]
Recently it was reported that members of miR-30 family are involved in myocardial extracellular matrix remo deling targeting connective tissue growth factors that are induced by TGF-β and endothelin [79]. [score:3]
J Cereb Blood Flow Metab 79 Duisters RF Tijsen AJ Schroen B Leenders JJ Lentink V 2009 miR-133 and miR-30 regulate connective tissue growth factor: implications for a role of microRNAs in myocardial matrix remo deling. [score:2]
To our knowledge, the role of miR-30 has not been studied in astrocytes. [score:1]
It is tempting to speculate a role of miR-30 in controlling apoptosis in astrocytes under hypoxic stress conditions and in induction of astrocyte proliferation and reactive gliosis through similar pathways as in cardiomyocytes. [score:1]
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[+] score: 10
The underlying mechanism might be related to the modulation of 18 upregulated and 14 downregulated miRNAs, in particular, miR-20a, miR-145, miR-30, and miR-98. [score:7]
Thus, involution was obtained by miChip analysis for four selected miRNAs that showed either high (miR-145) or low (miR-30) signal intensities, or high (miR-20a) or low (miRNA-98) differential expression values among the three groups. [score:3]
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20
[+] score: 10
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-26b, hsa-mir-29a, hsa-mir-30a, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, mmu-let-7g, mmu-let-7i, mmu-mir-15b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-130a, mmu-mir-138-2, mmu-mir-181a-2, mmu-mir-182, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-10a, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-181a-1, mmu-mir-297a-1, mmu-mir-297a-2, mmu-mir-301a, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, mmu-mir-106a, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-130a, hsa-mir-138-2, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-138-1, 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-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-34a, rno-mir-301a, rno-let-7d, rno-mir-344a-1, mmu-mir-344-1, rno-mir-346, mmu-mir-346, rno-mir-352, hsa-mir-181b-2, mmu-mir-10a, mmu-mir-181a-1, mmu-mir-29b-2, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-181c, mmu-mir-125b-1, hsa-mir-106b, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-34b, hsa-mir-34c, hsa-mir-301a, hsa-mir-30e, hsa-mir-362, mmu-mir-362, hsa-mir-369, hsa-mir-374a, mmu-mir-181b-2, hsa-mir-346, 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-10a, rno-mir-15b, rno-mir-26b, rno-mir-29b-2, rno-mir-29a, rno-mir-29b-1, rno-mir-29c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-34b, rno-mir-34c, rno-mir-34a, rno-mir-106b, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-130a, rno-mir-138-2, rno-mir-138-1, rno-mir-181c, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-181a-1, hsa-mir-449a, mmu-mir-449a, rno-mir-449a, mmu-mir-463, mmu-mir-466a, hsa-mir-483, hsa-mir-493, hsa-mir-181d, hsa-mir-499a, hsa-mir-504, mmu-mir-483, rno-mir-483, mmu-mir-369, rno-mir-493, rno-mir-369, rno-mir-374, hsa-mir-579, hsa-mir-582, hsa-mir-615, hsa-mir-652, hsa-mir-449b, rno-mir-499, hsa-mir-767, hsa-mir-449c, hsa-mir-762, mmu-mir-301b, mmu-mir-374b, mmu-mir-762, mmu-mir-344d-3, mmu-mir-344d-1, mmu-mir-673, mmu-mir-344d-2, mmu-mir-449c, mmu-mir-692-1, mmu-mir-692-2, mmu-mir-669b, mmu-mir-499, mmu-mir-652, mmu-mir-615, mmu-mir-804, mmu-mir-181d, mmu-mir-879, mmu-mir-297a-3, mmu-mir-297a-4, mmu-mir-344-2, 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-493, mmu-mir-504, mmu-mir-466d, mmu-mir-449b, hsa-mir-374b, hsa-mir-301b, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-879, mmu-mir-582, rno-mir-181d, rno-mir-182, rno-mir-301b, rno-mir-463, rno-mir-673, rno-mir-652, mmu-mir-466l, mmu-mir-669k, mmu-mir-466i, mmu-mir-669i, mmu-mir-669h, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-466j, mmu-mir-1193, mmu-mir-767, rno-mir-362, rno-mir-504, rno-mir-582, rno-mir-615, mmu-mir-3080, mmu-mir-466m, mmu-mir-466o, mmu-mir-466c-2, mmu-mir-466b-4, mmu-mir-466b-5, mmu-mir-466b-6, mmu-mir-466b-7, mmu-mir-466p, mmu-mir-466n, mmu-mir-344e, mmu-mir-344b, mmu-mir-344c, mmu-mir-344g, mmu-mir-344f, mmu-mir-374c, mmu-mir-466b-8, hsa-mir-466, hsa-mir-1193, rno-mir-449c, rno-mir-344b-2, rno-mir-466d, rno-mir-344a-2, rno-mir-1193, rno-mir-344b-1, hsa-mir-374c, hsa-mir-499b, mmu-mir-466q, mmu-mir-344h-1, mmu-mir-344h-2, mmu-mir-344i, rno-mir-344i, rno-mir-344g, mmu-let-7j, mmu-mir-30f, mmu-let-7k, mmu-mir-692-3, rno-let-7g, rno-mir-15a, rno-mir-762, mmu-mir-466c-3, rno-mir-29c-2, rno-mir-29b-3, rno-mir-344b-3, rno-mir-466b-3, rno-mir-466b-4
Such a situation occurred for miR-26b, miR-30, and miR-374 downregulation, and for miR-34, miR-301, and miR-352 upregulation [121]. [score:7]
These miRNAs (miR-15a, miR-30, miR-182, and miR-804) are involved in cell proliferation, apoptosis, inflammation, epithelial-mesenchymal transition, invasion, oncogene inhibition, and intercellular adhesion. [score:3]
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[+] score: 10
As depicted in Fig 6, among the miRNAs elevated in serum in our study, LPS has been shown to increase expression of miR-10a, miR-100, miR-508/511, miR-30c, and miR-125b in human fibroblast-like synoviocytes [41], increase expression of miR-146a in a human monocyte cell line [42], and increase miR-21 in cultured murine monocytes [43]. [score:5]
miR-421 and miR-30c inhibit SERPINE 1 gene expression in human endothelial cells. [score:5]
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[+] score: 9
According to this observation, Caruso et al. (2010) showed that, during the onset of pulmonary arterial hypertension (PAH) after hypoxia, there is a reduced Dicer expression leading to miR-22, miR-30, and let-7f down-regulation and, at the same time, to miR-322 and miR-451 up-regulation in two different PAH rat mo dels. [score:9]
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[+] score: 9
Disagreements extend to other cell death-related microRNAs that were reported by Liu [6] to demonstrate changes in expression that we were not able to detect (mir-137 and miR-672) or whose expression did not seem to change in the present study (miR-214, miR-30-3p, miR-235-3p, and miR-674-5p). [score:5]
In agreement with their results, we observed the downregulation of miR-127, miR-181a, miR-411, miR-99a, miR-34a, miR-30b, and miR-30c, which according to Liu [6] should lead to increased inflammation. [score:4]
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[+] score: 8
It was found to be targeted by multiple microRNAs in our analysis, including miR-143, miR-30 family members, miR-140, miR-27b, miR-125a-5p, miR-128ab, and miR-342-3p. [score:3]
Among the important genes were Lifr, Acvr1c, and Pparγ which were found to be targeted by microRNAs in our dataset like miR-143, miR-30, miR-140, miR-27b, miR-125a, miR-128ab, miR-342, miR-26ab, miR-181, miR-150, miR-23ab and miR-425. [score:3]
According to our in silico analysis, Ppar γ is likely regulated by microRNAs like let-7 family members, miR-30 family members, miR-27b, miR-23ab, miR-93, miR-25, miR-128ab, miR-320, and miR-135. [score:2]
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[+] score: 8
Other miRNAs from this paper: rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2
In this study, we constructed a PDGFR-β shRNA expression plasmid, in which PDGFR-β shRNA embedded in an miR30 -based context was driven by a CMV promoter. [score:3]
The PDGFR-β shRNA was inserted immediately into the miR30 -based shRNA expression system of the pCMR30 vector (Genechem, Shanghai, China) to generate a pCMV–shRNA–red fluorescent protein (RFP), in which PDGFR-β shRNA was driven by the CMV promoter and RFP was the reporter gene. [score:3]
To generate pCMV–shRNA–LacZ, the fragment containing miR30 -based PDGFR-β shRNA was PCR-cloned into the HindIII site of the pMIR-REPORT β-gal reporter control vector (Ambion, Austin, TX, USA), which supplies the β-gal reporter gene. [score:1]
As a negative control, we generated pCMV–NC–LacZ with miR30 -based PDGFR-β shRNA in pCMV–shRNA–LacZ replaced by negative control RNA. [score:1]
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[+] score: 8
Picking out 7 miRNAs associated with heart failure and taking statistical analysis, we found that Shenfu injection could significantly downregulate the levels of rno-miR-30c-1-3p, rno-miR-125b-5p, rno-miR-133a-5p, rno-miR-199a-5p, rno-miR-221-3p, rno-miR-146a-5p, and rno-miR-1-3p (Figure 5(b)). [score:4]
Picking out 7 miRNAs associated with heart failure and taking statistical analysis, our data reveal that Shenfu injection could significantly downregulate the levels of rno-miR-30c-1-3p, rno-miR-125b-5p, rno-miR-133a-5p, rno-miR-199a-5p, rno-miR-221-3p,rno-miR-146a-5p, and rno-miR-1-3p. [score:4]
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27
[+] score: 7
Members of the miRNA-30 family are highly expressed in the kidneys of humans and rats [44] and changes in their expression may result in glomerular disease [45]. [score:7]
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[+] score: 7
It is noteworthy that miR-1, miR-133, miR-30, miR-208a, miR-208b, mir-499, miR-23a, miR-9 and miR-199a have previously been shown to be functionally involved in cardiovascular diseases such as heart failure and hypertrophy [40], [41], [42], [43], [44], and have been proposed as therapeutic- or disease-related drug targets [45], [46]. [score:7]
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[+] score: 6
Shen Y. Shen Z. Miao L. Xin X. Lin S. Zhu Y. Guo W. Zhu Y. Z. miRNA-30 family inhibition protects against cardiac ischemic injury by regulating cystathionine-γ-lyase expression Antioxid. [score:6]
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[+] score: 5
The altered regulation of miR-30a is also of interest because the miR-30 family is well studied but has not previously been reported as being involved in vascular changes after SAH. [score:2]
Duisters RF, Tijsen AJ, Schroen B, Leenders JJ, Lentink V, van der Made I, et al. miR-133 and miR-30 regulate connective tissue growth factor: implications for a role of microRNAs in myocardial matrix remo deling. [score:2]
The miR-30 family members are known for their role in angiogenesis-related myocardial matrix remo deling via their interaction with connective tissue growth factor [37]. [score:1]
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[+] score: 5
Notably, a panel of 11 Runx2 -targeting miRNAs (miR-23a, miR-30c, miR-34c, miR-133a, miR-135a, miR-137, miR-204, miR-205, miR-217, miR-218, and miR-338) is expressed in a lineage-related pattern in mesenchymal cell types [20]. [score:5]
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[+] score: 5
In addition to the aforementioned study of the expression of mir-30d, there were several other expression profiling reports suggesting the involvement of mir-30 family in diabetes or adipogenesis [47]– [49]. [score:5]
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33
[+] score: 5
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-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-33a, hsa-mir-98, hsa-mir-29b-1, hsa-mir-29b-2, mmu-let-7g, mmu-let-7i, mmu-mir-27b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-126a, mmu-mir-133a-1, mmu-mir-135a-1, mmu-mir-141, mmu-mir-194-1, mmu-mir-200b, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-203a, hsa-mir-211, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-200b, mmu-mir-300, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-30b, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-141, hsa-mir-194-1, 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-21a, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-27a, mmu-mir-98, mmu-mir-326, rno-mir-326, rno-let-7d, rno-mir-343, rno-mir-135b, mmu-mir-135b, hsa-mir-200c, mmu-mir-200c, mmu-mir-218-1, mmu-mir-218-2, mmu-mir-33, mmu-mir-211, mmu-mir-29b-2, mmu-mir-135a-2, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-326, hsa-mir-135b, mmu-mir-133a-2, 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-21, rno-mir-26b, rno-mir-27b, rno-mir-27a, rno-mir-29b-2, rno-mir-29a, rno-mir-29b-1, rno-mir-29c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-33, rno-mir-98, rno-mir-126a, rno-mir-133a, rno-mir-135a, rno-mir-141, rno-mir-194-1, rno-mir-194-2, rno-mir-200c, rno-mir-200a, rno-mir-200b, rno-mir-203a, rno-mir-211, rno-mir-218a-2, rno-mir-218a-1, rno-mir-300, hsa-mir-429, mmu-mir-429, rno-mir-429, hsa-mir-485, hsa-mir-511, hsa-mir-532, mmu-mir-532, rno-mir-133b, mmu-mir-485, rno-mir-485, hsa-mir-33b, mmu-mir-702, mmu-mir-343, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, hsa-mir-300, mmu-mir-511, rno-mir-466b-1, rno-mir-466b-2, rno-mir-532, rno-mir-511, mmu-mir-466b-4, mmu-mir-466b-5, mmu-mir-466b-6, mmu-mir-466b-7, mmu-mir-466b-8, hsa-mir-3120, rno-mir-203b, rno-mir-3557, rno-mir-218b, rno-mir-3569, rno-mir-133c, rno-mir-702, rno-mir-3120, hsa-mir-203b, mmu-mir-344i, rno-mir-344i, rno-mir-6316, mmu-mir-133c, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-30f, mmu-let-7k, mmu-mir-3569, rno-let-7g, rno-mir-29c-2, rno-mir-29b-3, rno-mir-466b-3, rno-mir-466b-4, mmu-mir-203b
We used TargetScan and miRanda database queries to obtain miRNAs, which had higher targeting combined with N4bp2, namely, miR-200, miR-429, miR-29 and miR-30. [score:5]
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34
[+] score: 5
After normalizing the signal intensities for all miRNA expression levels, miR-124-3p, miR-9a-3p, miR-34a-5p, miR-9a-5p, miR-125b-5p, miR-let-7c-5p, miR-29a-3p, miR-23b-3p, miR-451-5p, and miR-30c-5p were the miRNAs expressed at the highest levels (Figure  1). [score:5]
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[+] score: 5
For instance, we observed a decrease in the levels of 5 miRNA with predicted target sites in the Foxa1 3′UTR (miR-106b, miR-194, miR-30c, miR-30b-5p and miR-20a) along with increased Foxa1 mRNA expression on methamphetamine exposure. [score:5]
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36
[+] score: 5
Similarly, some down-regulated miRNAs, such as miR-326 and miR-30c, were also associated with no change in their primary transcripts (Figure 5D and E). [score:4]
In the case of miR-30c and miR-128a, the mature miRNAs map to two different primary transcripts. [score:1]
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37
[+] score: 5
There were no significant changes in the expression of miR-15, miR-30, and miR-133a between healthy subjects and patients with burn injury. [score:3]
MiR-195, let-7e, miR-15, miR-133a, and miR-30 did not show any significant difference between burn rats and sham rats (Figure 1A) (P>0.05). [score:1]
MiR-15, miR-133a, and miR-30 also had P [CT] > 0.75. [score:1]
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38
[+] score: 4
Other miRNAs from this paper: rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2
Previous studies have demonstrated that angiotensin II could induce the down-regulation of miR-30 [41], increase mitochondria oxidative stress [42], thereby causing myocardium autophagy, which indicated that RAS activation could result in the cellular autophagy. [score:4]
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39
[+] score: 4
miR-30 regulates mitochondrial fission through targeting p53 and the dynamin-related protein-1 pathway. [score:4]
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40
[+] score: 4
Other miRNAs from this paper: rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2
As previously reported [14], short hairpin RNAs targeting firefly luciferase (accession number M15077, non-mammalian control, luciferase shRNA), rat VEGF [164] (accession number AF260425, VEGF [164] shRNA) and rat VEGFA (accession number NM_031836, VEGF-A shRNA) were embedded into a microRNA (miR-30) context. [score:3]
The miR-30/shRNAs were cloned into a lentiviral transfer vector under transcriptional control of a CD44 promoter (pFmCD44.1 GW), with green fluorescent protein (GFP) as a reporter gene. [score:1]
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41
[+] score: 4
PE + miR30 inhibitor. [score:3]
PE + miR30 mimics, [&&]p < 0.01 vs. [score:1]
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42
[+] score: 3
Other miRNAs from this paper: rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2
Column 4 is a similar co transfection with another shRNA vector based on the mir-30 system that contains the same shRNA targeting sequence as the shRNA shown in column 3 experiments. [score:3]
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43
[+] score: 3
Patel N. Tahara S. M. Malik P. Kalra V. K. Involvement of mir-30c and mir-301a in immediate induction of plasminogen activator inhibitor-1 by placental growth factor in human pulmonary endothelial cells Biochem. [score:3]
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44
[+] score: 3
Other miRNAs from this paper: rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2
The template “miRNA30‐like” DNA oligonucleotides targeting two positions of NR1 mRNAs (shRNAmir1 and shRNAmir2) were ligated into the XhoI/ MluI sites in the pGIPZ‐shRNAmir vector (Open Biosystems). [score:3]
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45
[+] score: 3
The reference genes utilised were miRNAs with stable expression across samples according to BestKeeper: miR-22, miR-30a, miR-30c, miR-30e and miR-100. [score:3]
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46
[+] score: 3
As shown in Table 2, we found increased expression of liver specific miRNAs in transdifferentiated hepatocytes, including miR-122a, miR-21, miR-22, miR-182, miR-29 and miR-30. [score:3]
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47
[+] score: 3
MiR-29, miR-133 and miR-30c are the most strongly fibrosis -associated miRNAs targeting a number of extracellular-matrix-related mRNAs [31], [32]. [score:3]
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[+] score: 3
Specifically, some studies have focused on the roles of miRNAs in the protective effects of fish oil or omega-3 PUFAs against metabolic syndrome and found that the intake of fish oil or DHA/EPA can modify the expression of miR-30b and miR-378 [49], miR-33a and miR-122 [50], miR-107 [51], miR-192, and miR-30c [52]. [score:3]
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49
[+] score: 2
Relative expression levels of the selected miRNAs and mRNAs were depicted in Figure 3. Consistent with the microarray data, real-time PCR confirmed that, compared with controls, rno-miR-132-3p, rno-miR-181a-1-3p, rno-miR-222-3p, and rno-miR-351-5p were significantly increased, while rno-miR-192-3p, rno-miR-194-5p, rno-miR-29c-3p, rno-miR-185-5p, and rno-miR-30c-5p were significantly decreased in stone-forming rat kidneys. [score:2]
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50
[+] score: 2
The target miRNAs (and corresponding assay numbers) were: rno-miR-23a (000399), rno-miR-26b (000407), rno-miR-30-5p (000420), rno-miR-101b (002531), rno-miR-125b-5p (000449), rno-miR-379 (001138) and rno-miR-431 (001979). [score:2]
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51
[+] score: 2
We designed and cloned into the pcPURhU6 vector the hairpin-type RNAs with si-6 sequence (pcPURhU6 si-6) with the 19-21 base pair (bp) stems and with various loops: (1) pcPURhU6 si-6 (21 bp)-miR26, (2) si-6 (19 bp) with 9-nt UUCAAGAGA loop [28], (3) si-6 (21 bp) with 9-nt UUCAAGAGA loop, (4) si-6 (21 bp) with 10-nt CUUCCUGUCA (loop from miRNA23), and (5) si-6 (21 bp) with 19-nt UAGUGAAGCCACAGAUGUA (loop from miRNA30) (see Figure 3). [score:1]
Constructs 4 and 5 with miRNA-origin loops miRNA23 and miRNA30, respectively, demonstrated moderate silencing activity, lowering BACE1 mRNA by 27% and 38%, respectively. [score:1]
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52
[+] score: 2
Moreover, the fine coordination of activity of the transmembrane receptor smoothened by the miR-30 family allows the correct specification and differentiation of distinct muscle cell types during zebrafish embryonic development 41. [score:2]
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53
[+] score: 2
Duisters R. F. Tijsen A. J. Schroen B. Leenders J. J. Lentink V. van der Made I. Herias V. van Leeuwen R. E. Schellings M. W. Barenbrug P. miR-133 and miR-30 regulate connective tissue growth factor: Implications for a role of micrornas in myocardial matrix remo deling Circ. [score:2]
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54
[+] score: 2
The amiRNAs represent a type of shRNAs in which a siRNA sequence is embedded into a native microRNA scaffold [30], most commonly into that of miR-30 [30], [31] or miR-155 [32], [33]. [score:1]
We confirmed that the silencing efficiency of amiR155-PLBr used here was comparable to that using a miR-30 scaffold (data not shown). [score:1]
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55
[+] score: 2
Duisters R. F. Tijsen A. J. Schroen B. Leenders J. J. Lentink V. van der Made I. Herias V. van Leeuwen R. E. Schellings M. W. Barenbrug P. miR-133 and miR-30 regulate connective tissue growth factor: Implications for a role of microRNAs in myocardial matrix remo deling Circ. [score:2]
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56
[+] score: 1
All short hairpin RNAs (shRNAs) were generated using a mir-30 -based design method, which has been previously described [25]. [score:1]
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57
[+] score: 1
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-27b, 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-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
Interestingly, among the conserved miRNAs found in all epididymal regions, we identified 8/14 and 4/7 members of the let-7 family (let-7a—let-7f, let-7i) and miR-30 (miR-30a— miR-30d) family, respectively. [score:1]
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[+] score: 1
MiR-30C was computationally predicted to bind the 3′UTR of panda ADRA1D gene and miR-199a-5p to the 3′UTR of panda COMT gene (Figure 3 & Figure S2). [score:1]
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59
[+] score: 1
Lentiviral vectors encoding miR-20a or a control sequence within a common miR-30 backbone have been previously described [16]. [score:1]
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60
[+] score: 1
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-16-1, hsa-mir-17, hsa-mir-21, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-30a, hsa-mir-31, hsa-mir-96, hsa-mir-99a, hsa-mir-16-2, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-182, hsa-mir-183, hsa-mir-211, hsa-mir-217, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-221, hsa-mir-222, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-132, hsa-mir-143, hsa-mir-145, hsa-mir-191, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-184, hsa-mir-190a, hsa-mir-195, rno-mir-322-1, rno-let-7d, rno-mir-335, rno-mir-342, rno-mir-135b, hsa-mir-30c-1, hsa-mir-299, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-379, hsa-mir-382, hsa-mir-342, hsa-mir-135b, hsa-mir-335, 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-15b, rno-mir-16, rno-mir-17-1, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-24-1, rno-mir-24-2, rno-mir-25, rno-mir-26a, rno-mir-26b, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-31a, rno-mir-96, rno-mir-99a, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-126a, rno-mir-132, rno-mir-143, rno-mir-145, rno-mir-183, rno-mir-184, rno-mir-190a-1, rno-mir-191a, rno-mir-195, rno-mir-211, rno-mir-217, rno-mir-218a-2, rno-mir-218a-1, rno-mir-221, rno-mir-222, rno-mir-299a, hsa-mir-384, hsa-mir-20b, hsa-mir-409, hsa-mir-412, hsa-mir-489, hsa-mir-494, rno-mir-489, rno-mir-412, rno-mir-543, rno-mir-542-1, rno-mir-379, rno-mir-494, rno-mir-382, rno-mir-409a, rno-mir-20b, hsa-mir-542, hsa-mir-770, hsa-mir-190b, hsa-mir-543, rno-mir-466c, rno-mir-17-2, rno-mir-182, rno-mir-190b, rno-mir-384, rno-mir-673, rno-mir-674, rno-mir-770, rno-mir-31b, rno-mir-191b, rno-mir-299b, rno-mir-218b, rno-mir-126b, rno-mir-409b, rno-let-7g, rno-mir-190a-2, rno-mir-322-2, rno-mir-542-2, rno-mir-542-3
These include rno-miR-195, rno-miR-125a-5p, rno-let-7a, rno-miR-16, rno-miR-30b-5p, rno-let-7c, rno-let-7b, rno-miR-125b-5p, rno-miR-221, rno-miR-222, rno-miR-26a, rno-miR-322, rno-miR-23a, rno-miR-191, rno-miR-30 family, rno-miR-21, rno-miR-126, rno-miR-23b, rno-miR-145 and rno-miR-494. [score:1]
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