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12 publications mentioning rno-mir-483

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-483. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

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[+] score: 324
We found that overexpression of pre-miR-483 inhibits CCl [4] -induced liver fibrosis by targeting platelet-derived growth factor-β (PDGF-β) and tissue inhibitor of metalloproteinase 2 (TIMP2) in the activation of HSCs. [score:9]
This effect might depend on at least two following pathways: (1) miR-483 inhibits the activation of HSCs by directly suppressing PDGF-β and TIMP2; and (2) HCs, which overexpress miR-483, might help to reduce the activation of HSCs in miR-483 transgenic mice. [score:8]
The suppressor of cytokine signalling 3 (Socs3) is a verified functional target of miR-483-5p and, was down-regulated in TG mouse livers (Fig.   S10D and E). [score:8]
α-SMA was down-regulated by overexpression of miR-483 at the translational level (Fig. 3D). [score:8]
To verify the targets of miR-483 in the activation of HSCs, we first determined the expression of the potential targets PDGF-β and TIMP2 after transfection with the miR-483 mimics or control into LX-2 cells, human HSC cell line. [score:7]
A study by Veronese et al. showed that miR-483-3p is down-regulated in HCC by its own transcriptional region [19], and Wang et al. reported that miR-483 is down-regulated in HCC [20]. [score:7]
Overexpression of miR-483-5p in HCs reduces the expression of artificial target in HSCs. [score:7]
Altogether, our results show that overexpression of miR-483 inhibits liver fibrosis, in part by suppressing PDGF-β and TIMP2 during the activation of HSCs in transgenic mice. [score:7]
The expression of TIMP2 and PDGF at translational level after activition by TGF and overexpress miR-483. [score:7]
To further test whether the putative miR-483 target sequences in the PDGF-β and TIMP2 3′ UTRs mediate the translational repression of PDGF-β and TIMP2 in mice, we inserted the mice 3′ UTR of either the PDGF-β or TIMP2 transcript, which contained either the binding sequences (56-76, 80-101, 939-959 for PDGF-β and 252-273, 1324-1347, 1992-2015 for TIMP2, See Fig.   S4) or a mutant sequence, into a luciferase expression plasmid (Fig. 4E). [score:7]
Although miR-483 was identified in foetal liver [22] and overexpressed in liver cancer [14, 15], it is down-regulated in activated rat primary HSCs [18]. [score:6]
Therefore, we focused on the role of miR-483 in human development and disease, particularly liver disease. [score:6]
PDGF-β and TIMP2 were down-regulated by miR-483 (Fig. 4B; Western blotting, Fig.   S2B), although TIMP2 cannot be predicted as th target of miR-483-3p. [score:6]
To further elucidate the inhibitory effect of miR-483 on liver fibrosis in miR-483 transgenic mice, we determined whether HCs that overexpress miR-483 could regulate the activation of HSCs. [score:6]
In addition, miR-483 is up-regulated in approximately half of human tumours [14], including adrenocortical carcinoma and HCC [15, 16], and its oncogenic targets, PUMA, CTNNB1, IGF1R, have been identified. [score:6]
Our data suggest that overexpression of miR-483 regulates liver fibrosis by inhibiting the activation of HSCs in transgenic mice. [score:6]
Overexpression of miR-483 reduced the up-regulation of α-SMA and collagen1α1 in mouse liver induced by CCl [4]. [score:6]
However, miR-483-5p, but not miR-483-3p, is down-regulated only in thioacetamide (TAA) -induced liver fibrosis, which may result from its own transcriptional-regulation region [19] or the difference between TAA and CCl [4]. [score:5]
A direct co-culture assay was performed; the results showed that overexpression of miR-483 in HL7702 cells could reduced the expression of GFP-S-483 in LX-2 (Fig.   S9). [score:5]
Figure 2Overexpression of pre-miR-483 inhibits CCl [4] -induced liver fibrosis in transgenic mice. [score:5]
Our results demonstrate that overexpression of miR-483 in HCs may inhibit liver fibrosis for future gene therapy. [score:5]
Overexpression of pre-miR-483 in vivo inhibited CCl [4] -induced liver fibrosisTo evaluate the role of miR-483 in vivo, we engineered pre-miR-483 transgenic mice, the expression of which is driven by the CAG promoter (Fig. 1B). [score:5]
Overexpression of miR-483 decreased the translation of TIMP2 and PDGF-β. [score:5]
In summary, our results reveal that miR-483-5p/3p overexpression inhibits the activation of HSCs in the liver both in vitro and in vivo. [score:5]
Collectively, these data demonstrate that overexpression of pre-miR-483 may inhibit liver fibrosis and that miR-483 is a protective factor against liver fibrosis. [score:5]
miR-483-3p and miR-483-5p reduced the expression of TIMP2 and PDGF-β by targeting their UTR; * P < 0.05, ** P < 0.01. [score:5]
This suggested an indirect effect that miR-483-3p regulated the expression of TIMP2 in LX-2 cells. [score:5]
Overexpression of pre-miR-483 in vivo inhibited CCl [4] -induced liver fibrosis. [score:5]
However, recently, miR-483 was reported to be down-regulated in activated rat primary HSCs induced by choline -deficient ethionine supplementation [18]. [score:4]
Although our finding demonstrated the down-regulation and function of miR-483 in mouse liver fibrosis, carcinogenesis was also induced. [score:4]
Down-regulation of miR-483-5p and miR-483-3p in CCl4- or TAA -induced liver fibrosis in mice. [score:4]
miR-483 and miR-675 appear to be a pair of intragenic miRNAs that regulate the expression of this imprinting region. [score:4]
miR-483 was reported to be down-regulated in activated rat primary HSCs. [score:4]
In addition, this study showed that miR-483-3p has its own upstream transcriptional-regulation region [19], and miR-483-5p and miR-483-3p present with differential expression patterns in developing human brains [23]. [score:4]
The variable expression of miR-483 causes the development of HCC from liver fibrosis, which has been previously suggested to be a continuous process. [score:4]
Next, we identified the targets of miR-483 in this regulatory process. [score:4]
Therefore, we determined that the level of miR-483 is down-regulated during CCl [4] -induced liver fibrosis in mice. [score:4]
To further elucidate the molecular mechanism by which miR-483 regulates the activation of HSCs, we used bioinformatics software to predict the targets of miR-483. [score:4]
However, dysexpression of miR-483 occurred during this continuous process. [score:3]
Interestingly, miR-483 is embedded in the second intron of the Igf2 gene, which is overexpressed in liver fibrosis and HCC [24]. [score:3]
miR-483-5p and miR-483-3p expression is reduced in CCL [4] -induced mouse liver fibrosismiR-483-5p and miR-483-3p originate from the pre-miR-483 locus. [score:3]
Han et al. reported that the target of miR-483-3p, hMECP2, which contains a long UTR, is unique to humans [23]. [score:3]
Finally, we found overexpression of miR-483 induced mice liver carcinogenesis. [score:3]
miR-483-5p and miR-483-3p cooperatively target PDGF-β and TIMP2. [score:3]
Overexpression of miR-483 may cause DEN -induced carcinogenesis (Fig.   S10B and C). [score:3]
Pre-miR-483 was cloned into the EcoR I site of a pCAGGs expression vector, which contained the chicken β-actin promoter. [score:3]
The predicted targets of miR-483 include pro-fibrosis and anti-fibrosis genes in human and mice (Table  S1). [score:3]
miR-483-5p and miR-483-3p inhibit TGF-β stimulated HSC LX-2 cells. [score:3]
In our miR-483 transgenic mice, ubiquitous expression of miR-483 resulted from the CAG promoter. [score:3]
In this study, we provide evidence for an anti-fibrosis role of miR-483-5p and miR-483-3p during the progression of liver disease. [score:3]
Figure 3miR-483-5p and miR-483-3p inhibit transforming growth factor-β (TGF-β) stimulated LX-2 cells. [score:3]
Differential expression of miR-483-5p in several cell lines. [score:3]
However, the dysexpression of miR-483 in liver fibrosis and HCC might result from other mechanism, such as H19 gene and its intragenic miRNA miR-675. [score:3]
However, we failed to observe the distinguished role of overexpression of miR-483 in HL7702 cells on the α-SMA protein level in LX-2 by a direct co-culture assay (Fig.   S6C). [score:3]
Therefore, we engineered pre-miR-483 overexpressing transgenic mice under the control of the cytomegalovirus early enhancer/chicken β-actin (CAG) promoter. [score:3]
In addition, PDGF-β and TIMP2 protein expression was decreased in the livers of the CCl [4] -treated miR-483 transgenic mice compared to the wild-type littermates (Fig. 4C and D), which is consistent with the conclusion that miR-483 acts as a negative regulator of PDGF-β and TIMP2 in vitro. [score:3]
The transgenic mouse liver overexpressed miR-483-5p and miR-483-3p (Fig. 1C and D). [score:3]
This result suggests that overexpression of miR-483 for 12 months promotes HCC carcinogenesis (Fig.   S10A). [score:3]
First, stimulation of the human HSC cell line LX-2 with recombinant TGF-β, a major cytokine involved in HSC activation (Fig. 3A and B), led to an increase in TIMP2 and PDGF-β (Fig.   S2A) and significant decrease in miR-483 expression (Fig. 3C). [score:3]
miR-483-5p and miR-483-3p expression is reduced in CCL [4] -induced mouse liver fibrosis. [score:3]
The role of overexpression of miR-483 in HCs on the activation of HSCs in the miR-483 transgenic mice needs further research. [score:3]
Finally, we built a reporter plasmid containing a reporter gene GFP (green fluorescent protein) and a double copy anti-sense sequence of miR-483-5p (Sponges-miR-483-5p, S-483) downstream of GFP gene which could be served as an artificial target of miR-483-5p. [score:3]
Potential targets of miR-483 predicted by bioinformatics software. [score:3]
Both miR-483-5p and miR-483-3p showed significantly lower expression compared to the control animals. [score:2]
Moreover, miR-483 belongs to the Igf2-H19 locus, which is an important imprinting region in development and carcinogenesis [29]. [score:2]
Dysregulation of miR-483 in mice liver carcinogenesis. [score:2]
miR-483-5p and miR-483-3p originate from the pre-miR-483 locus. [score:1]
We explored the potential interaction between HCs and HSCs in miR-483 transgenic mice. [score:1]
Interestingly, miR-483 is conserved in both humans and mice; however, the binding sites in the UTR of TIMP2 are not conserved (Fig.   S3). [score:1]
The presence of miR-483 was determined 48 hrs after the co-culture of HCs and HSCs after the cells were washed three times with PBS (2 ml/wash). [score:1]
As an intragenic miRNA, miR-483 may affect the function of its host gene. [score:1]
These data suggest that miR-483 is a partner of its host gene Igf2. [score:1]
Interestingly, the binding sequence of the UTR (1324-1347) seemed more important than the UTR (1992-2015) for miR-483-5p in TIMP2 (Fig. 4F). [score:1]
These results are consistent with the role of miR-483 in vivo. [score:1]
We then transfected either miR-483 or a control sequence into the TGF-β stimulated LX-2 cells. [score:1]
In our earlier studies, miR-483 was identified as an oncogenic factor in cancer cells, which is similar to its host gene Igf2 [17]. [score:1]
In our current study, miR-483 and the host gene play different roles. [score:1]
miR-483 was cloned between the two EcoR I sites, which puts the transgene under the control of the CAG promoter. [score:1]
Our findings address the function of miR-483 in liver fibrosis. [score:1]
To evaluate the role of miR-483 in vivo, we engineered pre-miR-483 transgenic mice, the expression of which is driven by the CAG promoter (Fig. 1B). [score:1]
Because we observed the inhibition of α-SMA in miR-483 transgenic mice, we investigated the role of miR-483 in the activation of HSCs. [score:1]
miR-483-5p and miR-483-3p were identified from a human embryonic liver and are generated from the same pre-cursor miRNA, which is derived from the second intron of the insulin-like growth factor 2 gene (Igf2) [11]. [score:1]
However, further studies are necessary to determine the mechanism by which miR-483 is delivered during liver fibrosis in the transgenic mice. [score:1]
Spontaneous tumours in miR-483 transgenic mice. [score:1]
Although our results suggested an intercellular transfer of miR-483 between HL7702 and LX-2 cells, we still lack sufficient evidence of the role of miR-483 in different cells. [score:1]
The transfection of the fluorescently labelled miR-483 was performed in the dark. [score:1]
The secretion of miR-483 was observed after the culture media was changed 48 hrs after the transfection of fluorescently labelled miR-483 after the cells were washed three times with PBS. [score:1]
We first choose the CAG promoter for the transgenic mice because miR-483 has lbeen detected in the liver tissue in previous studies. [score:1]
Until recently, genetically modified animals for functional miR-483 research were not available. [score:1]
Our previous study showed that miR-483-5p promoted the proliferation of a mouse HCC cell line [17]. [score:1]
White characters indicate the pre-miR-483 sequence, black background indicates homology, and grey background indicates different nucleotides. [score:1]
Because fibrosis can progress to HCC, we detected spontaneous tumours in the miR-483 transgenic mice. [score:1]
However, miR-483 was not an oncogenic factor in human umbilical vein endothelial cells [28]. [score:1]
Interestingly, the putative miR-483 binding sites in the 3′ UTR of the PDGF-β mRNA in both humans and mice share multi -binding sites in each UTR, but not in TIMP2 (Fig. 4A, Fig.   S3). [score:1]
Increasing amounts of miR-483 resulted in a decrease in luciferase activity, whereas the control sequence had no effect (Fig. 4F and G). [score:1]
The LX-2 cells (0.5 × 10 [5] cells per well) were seeded in the lower 3.5-cm plates, and the HL7702 cells (the 1.0 × 10 [5] cells per well) with transfected miR-483 were seeded in the upper transwell inserts. [score:1]
To determine the level of miR-483 in liver fibrosis in vivo, we used the well-established carbon tetrachloride (CCl [4]) treatment mo del to induce hepatic fibrosis in mice (Fig.   S1A). [score:1]
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Three miRNAs (upregulated miR-483 and downregulated let-7e and miR-199a) exhibited significantly fold changes (Fig.   1). [score:7]
All data are expressed as mean ± SEM Based on multiple databases (TargetScan, Microcosm Targets and RNA22-HAS), SRF was predicted to have a putative miR-483-3p binding sites within its 3′UTR (Fig.   4a, b). [score:7]
miR-483-3p is upregulated in EPCs from DVT patients, and it targets SRF to decrease EPCs migration and tube formation and increase apoptosis in vitro, while decrease EPCs homing and thrombus resolution in vivo. [score:6]
Indeed, previous study reported that miR-483-5p directly targeted SRF in human umbilical vein endothelial cells and inhibited angiogenesis in vitro [43]. [score:6]
Our results showed that the expression of miR-483-3p was significantly upregulated (Fig.   1, fivefold increase, P < 0.05), indicating the potential role of miR-483-3p in DVT. [score:6]
In conclusion, this study shows that miR-483-3p is upregulated in EPCs from DVT patients and it impairs EPCs function via its target SRF. [score:6]
Here we reported the upregulation of miR-483-3p in DVT patients and demonstrated that ectopic expression of miR-483-3p attenuated the migration, tube formation and increased the apoptosis of EPCs via SRF in vitro. [score:6]
To clarify the role of miR-483-3p in EPCs, we employed miR-483-3p agomir and antagomir to overexpress and inhibit miR-483-3p in EPCs. [score:5]
To confirm the ability of miR-483-3p to inhibit SRF expression, we transfected EPCs with miR-483-3p agomir and antagomir. [score:5]
Our results confirmed that SRF was a target of miR-483-3p and the suppression of SRF by miR-483-3p was involved in the effects of miR-483-3p on EPCs function. [score:5]
To further confirm that miR-483-3p modulated EPCs function by targeting SRF, we performed rescue experiments by co-transfection of miR-483-3p agomir and SRF expression vector in EPCs, and EPCs showed similar trend of cell migration, tube formation and apoptosis as controls (Fig.   5a–c). [score:5]
To overexpress and knockdown miR-483-3p, agomir and antagomir of miR-483-3p were transfected into EPCs using Lipofectamine 3000 (Invitrogen, CA, USA) according to the manufacturer’s instructions. [score:4]
To elaborate putative mechanism by which miR-483-3p regulates EPCs function, we employed bioinformatics tool and molecular biology method to identify target gene. [score:4]
The migration, angiogenic potential and apoptosis of EPCs were positively regulated by SRF, and the suppression of SRF by miR-483-3p contributed to the effects of miR-483-3p on EPCs function. [score:4]
Taken together, our data suggest that miR-483-3p plays an important role in EPCs dysfunction, and upregulated miR-483-3p in EPCs from DVT contributes to impaired EPCs function, which is likely due to decreased SRF. [score:4]
We identified miR-483-3p as a candidate miRNA upregulated in EPCs from DVT patients. [score:4]
The upregulation of miR-483-3p in EPCs from patients with DVT. [score:4]
Moreover, we identified serum response factor (SRF) as the target of miR-483-3p, and showed that SRF knockdown decreased the migration and tube formation while increased the apoptosis of EPCs. [score:4]
In addition, DVT patients (n = 10) and healthy control subjects (n = 10) were included to verify the upregulation of miR-483-3p in EPCs from DVT patients by quantitative real-time PCR (Fig.   4g). [score:4]
First, miR-483-3p expression was increased in EPCs derived from patients with DVT. [score:3]
health control)To confirm that SRF is a direct target of miR-483-3p, we performed luciferase reporter assay and found decreased luciferase activity after a 395 bp region of 3′-UTR SRF was cloned into the luciferase report vector (Fig.   4c, d). [score:3]
MiR-483-3p sponge lentivirus virions totally silenced the expression of miR-483-3p (Fig.   6c). [score:3]
Putative binding sites of miR-483-3p in the SRF 3′UTR predicted by TargetScan among different mammalian species. [score:3]
Inhibition of miR-483-3p promoted thrombus recanalization and resolution. [score:3]
Overexpression of miR-483-3p decreased migration and angiogenic potential of EPCs while increased apoptosis of EPCs. [score:3]
c The relative expression of miR-483-3p after infection with lenti-vector control, lenti-483-3p and lenti-483-3p sponge. [score:3]
In addition, miR-483-3p inhibition led to enhanced ability of homing and thrombus resolution of EPCs in rat mo del of venous thrombosis. [score:3]
These data suggest that miR-483-3p might be employed as a therapeutic target in the treatment of thrombus in the clinical practice. [score:3]
a SRF is a putative target of miR-483-3p. [score:3]
Moreover, we identified SRF as the target of miR-483-3p in EPCs. [score:3]
MiR-483-3p regulates EPCs function by targeting SRF. [score:3]
b Putative binding sites of hsa-miR-483-3p in the human SRF 3′UTR (white sequences) predicted by TargetScan. [score:3]
Our results suggested that SRF could be the potential target of miR-483-3p. [score:3]
SRF is the target gene of miR-483-3p in EPCs. [score:3]
health control) To confirm that SRF is a direct target of miR-483-3p, we performed luciferase reporter assay and found decreased luciferase activity after a 395 bp region of 3′-UTR SRF was cloned into the luciferase report vector (Fig.   4c, d). [score:3]
Furthermore, the application of EPCs transfected with miR-483-3p inhibitor into the vein thrombosis rat mo del improved the thrombus recanalization and resolution. [score:3]
Fig.  4SRF is a validated target of miR-483-3p. [score:3]
MiR-483-3p is a potential therapeutic target in DVT treatment. [score:2]
IGF2 is involved in angiogenesis through the regulation of the IGF/IGF2R system, and miR-483-3p was an intronic miRNA within IGF2. [score:2]
MiR-483-3p inhibited EPCs homing. [score:2]
SRF-3′UTR mut indicates the SRF-3′UTR with mutation in miR-483-3P -binding site. [score:2]
Knockdown of miR-483-3P in EPCs via lentivirus -mediated miR-483-3p sponge. [score:2]
MiR-483-3p Endothelial progenitor cells Deep vein thrombosis Serum response factor Digital subtract angiography Deep vein thrombosis (DVT) occurs when a blood clot forms in the deep vein of human body, and is a common peripheral vascular disease that causes major morbidity and mortality in various medical conditions [1]. [score:2]
Moreover, we found that miR-483-3p regulated the migration and apoptosis of EPCs. [score:2]
In the present study, miR-483-5p emerges as a novel angio-miR that negatively regulates angiogenesis. [score:2]
Until now, the exact role of miR-483-3p in the function of EPCs has not been determined yet. [score:1]
EPCs transfected with pGLV3-H1-GFP-Puro-miR-483-3p were intravenously administrated into the rats. [score:1]
EPCs were infected with lentivirus -mediated vector control, miR-483-3p and miR-483-3p sponge, and the expression of the miR-483 cluster was measured by quantitative real-time PCR. [score:1]
EPCs transfected with miR-483-3p antagomir exhibited opposite behaviors on cell migration, tube formation and apoptosis (Fig.   3a–c). [score:1]
EPCs were transfected with miR-483-3p agomir or antagomir or negative control. [score:1]
In the present study, we reported several important findings on the role of miR-483-3p in EPCs. [score:1]
Furthermore, the thrombus weight of EPCs/miR-483-3p sponge group was even lower than that of EPCs/vector group (18.7 ± 6.1 vs. [score:1]
In addition, miR-483-3p sponge decreased the weight of thrombus (IVC + thrombus at harvest). [score:1]
To generate miR-483-3p sponge lentivirus virion, the sequences to miR-483-3p with mismatches at position 9–12 were constructed into the pGLV3-H1-GFP-Puro lentivirus infectious virions and used to infect EPCs. [score:1]
c Schematic graph of the constructed reporter plasmid containing putative binding sites of hsa-miR-483-3p in the SRF 3′UTR. [score:1]
g miR-483-3p expression was measured in healthy control and patients with DVT by quantitative real-time PCR. [score:1]
showed that SRF protein level was significantly increased after miR-483-3p sponge treatment (Fig.   6d). [score:1]
In addition, we established a rat mo del of vein thrombosis and observed that transplantation with EPCs transfected with miR-483-3p displayed increased homing ability and improved the thrombus recanalization and resolution in vivo. [score:1]
EPCs transfected with miR-483-3p agomir exhibited significantly decreased SRF protein level while EPCs tranfected with miR-483-3p antagomir exhibited increased SRF protein level (Fig.   4e). [score:1]
Then the rats were divided into four groups for cell transplantion via tail intravenous injection (n = 10): (A) blank control group (blank control) received same volume of cell culture medium; (B) EPCs/pGLV3-H1-GFP-Puro vector group (EPCs/vector) received 1.0 × 10 [6] EPCs transfected with pGLV3-H1-GFP-Puro control vector; (C) EPCs/pGLV3-H1- GFP-Puro-miR-483-3p group (EPCs/miR- 483-3p) received 1.0 × 10 [6] EPCs transfected with pGLV3-H1-GFP-Puro-miR-483-3p; (D) EPCs/pGLV3-H1-GFP-Puro-miR-483-3p sponge group (EPCs/miR-483-3p sponge) received 1.0 × 10 [6] EPCs transfected with pGLV3-H1-GFP-Puro-miR-483-3p sponge. [score:1]
By using miR-483-3p agomir and antagomir, we demonstrated that miR-483-3p decreased the migration and tube formation while increased the apoptosis of EPCs. [score:1]
EPCs transfected with miR-483-3p agomir displayed decreased ability of migration (Fig.   3a), tube formation (Fig.   3b) and increased apoptosis (Fig.   3c). [score:1]
d SRF protein level was significantly increased after miR-483-3p sponge treatment. [score:1]
There were more nucleated cells and channels in EPCs/vector and EPCs/miR-483-3p sponge group than in control group on day 7 (Fig.   7c). [score:1]
EPCs were infected with the viruses and selected in the presence of 5 μg/ml puromycin (Sigma), and the green fluorescent protein (GFP) signal of the infected cells was detected under microscope, and the expression of the miR-483 cluster in EPCs was measured by quantitative real-time PCR. [score:1]
miR-483-3p agomir + SRF). [score:1]
Partial pre-miR-483 sequences flanked by EcoRI and AgeI restriction site were constructed into the H1 promoter of lentivirus infectious virions pGLV3-H1-GFP-Puro (GenePharma, Shanghai, China). [score:1]
e The protein level of SRF in EPC transfected with miR-483-3p agomir and antagomir. [score:1]
Moreover, we tested the efficacy of miR-483-3p modified EPCs in the treatment of vein thrombosis using a rat mo del. [score:1]
EPCs/miR-483-3p). [score:1]
However, additional target genes are likely to participate in the anti-angiogenic effect of miR-483-3p, which remain to be investigated in the near future. [score:1]
Tube length obtained from miR-483-3p antagomir transfected cells was set to 100. [score:1]
f The protein level of SRF in EPC transfected with miR-483-3p agomir and SRF, SRF siRNA. [score:1]
Each bar represents mean values ± SEM We constructed a miR-483-3p sponge consisted of a decoy vector containing tandem repeated miRNA binding sites downstream of GFP (Fig.   6a). [score:1]
Therefore, our present study extended previous findings on miR-483-SRF pathway from endothelial cells to EPCs. [score:1]
b Binding sites of miR-483-3p sponge. [score:1]
Binding sites for miR-483-3p were complementary in the seed region with a bulge at positions 9–12 to prevent RNA interference-type cleavage and degradation of the sponge RNA constructed into the pGLV3-H1-GFP-Puro lentivirus infectious virions (Fig.   6b). [score:1]
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3
[+] score: 15
Other miRNAs from this paper: mmu-mir-30a, mmu-mir-101a, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-132, mmu-mir-134, mmu-mir-135a-1, mmu-mir-138-2, mmu-mir-142a, mmu-mir-150, mmu-mir-154, mmu-mir-182, mmu-mir-183, mmu-mir-24-1, mmu-mir-194-1, mmu-mir-200b, mmu-mir-122, mmu-mir-296, mmu-mir-21a, mmu-mir-27a, mmu-mir-92a-2, mmu-mir-96, rno-mir-322-1, mmu-mir-322, rno-mir-330, mmu-mir-330, rno-mir-339, mmu-mir-339, rno-mir-342, mmu-mir-342, rno-mir-135b, mmu-mir-135b, mmu-mir-19a, mmu-mir-100, mmu-mir-139, mmu-mir-212, mmu-mir-181a-1, mmu-mir-214, mmu-mir-224, mmu-mir-135a-2, mmu-mir-92a-1, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-125b-1, mmu-mir-194-2, mmu-mir-377, mmu-mir-383, mmu-mir-181b-2, rno-mir-19a, rno-mir-21, rno-mir-24-1, rno-mir-27a, rno-mir-30a, rno-mir-92a-1, rno-mir-92a-2, rno-mir-96, rno-mir-100, rno-mir-101a, rno-mir-122, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-132, rno-mir-134, rno-mir-135a, rno-mir-138-2, rno-mir-138-1, rno-mir-139, rno-mir-142, rno-mir-150, rno-mir-154, rno-mir-181b-1, rno-mir-181b-2, rno-mir-183, rno-mir-194-1, rno-mir-194-2, rno-mir-200b, rno-mir-212, rno-mir-181a-1, rno-mir-214, rno-mir-296, mmu-mir-376b, mmu-mir-370, mmu-mir-433, rno-mir-433, mmu-mir-466a, rno-mir-383, rno-mir-224, mmu-mir-483, rno-mir-370, rno-mir-377, mmu-mir-542, rno-mir-542-1, mmu-mir-494, mmu-mir-20b, mmu-mir-503, rno-mir-494, rno-mir-376b, rno-mir-20b, rno-mir-503-1, mmu-mir-1224, mmu-mir-551b, mmu-mir-672, mmu-mir-455, mmu-mir-490, 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-504, mmu-mir-466d, mmu-mir-872, mmu-mir-877, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-872, rno-mir-877, rno-mir-182, rno-mir-455, rno-mir-672, mmu-mir-466l, mmu-mir-466i, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-466j, rno-mir-551b, rno-mir-490, rno-mir-1224, rno-mir-504, 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-466b-8, rno-mir-466d, mmu-mir-466q, mmu-mir-21b, mmu-mir-21c, mmu-mir-142b, mmu-mir-466c-3, rno-mir-322-2, rno-mir-503-2, rno-mir-466b-3, rno-mir-466b-4, rno-mir-542-2, rno-mir-542-3
DEX treatment up-regulated the expression of miRNA-483, miRNA-181a-1, miRNA-490 and miRNA-181b-1, while it down-regulated the levels of miR-122, miR-466b, miR-200b, miR-877, miR-296, miRNA-27a and precursor of miR-504. [score:9]
The expression of miRNA-483, miRNA-181a-1, miRNA-490 and miRNA and miRNA-181b-1 was up-regulated in response to dexamethasone treatment. [score:6]
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4
[+] score: 6
Comparing significantly deregulated miRNAs in the SL- and PH-group, we identified 10 miRNAs (rno-miR-100, rno-miR-105, rno-miR-1224, rno-miR-133a/b, rno-miR-383, rno-miR-466c, rno-miR-483, rno-miR-598-5p, and rno-miR-628) that showed similar expression changes in both groups at the same postoperative time point, while one miRNA (rno-miR-29a) was regulated in the opposite direction at the same time point. [score:6]
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5
[+] score: 3
Ferland-McCollough D Fernandez-Twinn DS Cannell IG David H Warner M Vaag AA Bork-Jensen J Brons C Gant TW Willis AE Siddle K Bushell M Ozanne SE Programming of adipose tissue miR-483-3p and GDF-3 expression by maternal diet in type 2 diabetesCell Death Differ. [score:3]
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6
[+] score: 3
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-30c-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, 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
1Proliferation, Invasion, Tumor suppression [63– 66] miR-344 ↓2.0 ↓3.2 NA miR-346 ↓2.4Proliferation [67, 68] miR-362 ↓2.3Proliferation, Invasion, Apoptosis [69– 76] miR-369 ↓2.8 ↓2.6 ↓2.1Aerobic glycolysis [77] miR-374 ↑3.0 ↓2.2 NA miR-449 ↑2.7 ↑2.4Proliferation [78– 81] miR-463 ↓2.7 NAmiR-466 [°] ↑2.4 ↑2.1 ↓3.5 NA miR-483 ↓3.2Apoptosis [82] miR-493 ↑2.1 ↓2.2Proliferation [83– 85] miR-499a ↓5.0 ↑2.3Proliferation [86] miR-504 ↓2.6 ↑2.0Proliferation, Apoptosis [87, 88] miR-579 ↑2.8 NAmiR-582 [^] ↑2.4Proliferation [89] miR-615 ↓2.1Proliferation, Invasion [90, 91] miR-652 ↑2.4Proliferation, EMT [92, 93] miR-669b ↓2.1 NA miR-669h ↓3.6 ↑2.3 NA miR-669i ↓2.3 NA miR-669k ↓7.2 ↓5. [score:3]
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7
[+] score: 3
This was associated with increased miR-483 expression in both rodents and humans and led to a reduction in the expandability of adipose tissue [7]. [score:3]
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8
[+] score: 2
control Function rno-miR-653-3p 37.56097561 Unknown rno-miR-3594-3p 9.31358885 Unknown rno-miR-483-3p 8.414634146 Anti-apoptotic oncogene, cardiovascular inflammation and remo delling rno-miR-92b-5p 8.096126255 Heart development and atrial fibrillation rno-miR-377-5p 4.84735544 Atrial fibrillation and structural remo delling rno-miR-341 4.764878049 Atrial fibrillation and TGF-β/Smad2/3 pathway rno-miR-21-3p 4.637785208 Cell proliferation and invasion. [score:2]
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9
[+] score: 1
Among the 11 miRNAs quantified, 4 were not modulated after 7 days or 2 months MI: miR-29b-3p, miR-338-3p, miR-133a and miR-483-3p interacting respectively with tropomyosin alpha-1 chain, pyruvate kinase PKM and phosphoglycerate mutase 1 (Fig.   1B–E). [score:1]
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10
[+] score: 1
9 miRNAs were present in two categories; 5 of them were common between Tables 1 and 2 (miR-181a-5p, miR-204-5p and miR-2137, miR-421-3p and miR-483-3p), two miRNAs were present in both Tables 2 and 3 (miR-148a-5p and piR-335-3p) and the remaining two miRNAs were classified both in Tables 1 and 3 (miR-137-3p and miR-455-3p). [score:1]
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11
[+] score: 1
The IGF2 intronic miR-483 selectively enhances transcription from IGF2 fetal promoters and enhances tumorigenesis. [score:1]
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12
[+] score: 1
miR-21, miR-223, miR-455-5p, miR-431 and miR-18 were significantly increased, while miR-138, miR-483 and miR-383 were significantly decreased following nerve transection. [score:1]
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