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9 publications mentioning ssc-mir-424

Open access articles that are associated with the species Sus scrofa and mention the gene name mir-424. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 294
Other miRNAs from this paper: ssc-mir-21
Our findings provide three major conclusions (Fig. 6e): (i) the downregulation of miR-424 facilitates proliferation and osteogenic differentiation via the upregulation of FGF2 in the context of oxidative stress, (ii) FOXO1 transcriptionally suppresses miR-424 expression, and (iii) FOXO1 enhances proliferation and osteogenic differentiation, at least partly, through the miR-424/ FGF2 pathway. [score:11]
Similarly, the positive effect of miR-424 downregulation on osteogenic differentiation was abrogated by FGF2 knockdown, as shown by the significantly attenuated mRNA expression levels of RUNX2 and ALP by FGF2 siRNA, even during treatment with the miR-424 inhibitor (Fig. 4g,h). [score:9]
To understand the underlying mechanism, we searched for potential targets for miR-424 in Targetscan, PicTar and miRBase using miRNA target prediction algorithms. [score:7]
The protein expression of FOXO1 at 3 days increased in response to miR-424 overexpression, but it was not significantly altered by the inhibition of miR-424 (Fig. 4c,d). [score:7]
In agreement with these observations, our present study elaborately demonstrates that miR-424 inhibits both the proliferation and osteogenic differentiation of hASCs, as shown by decreased OD490 values, ALP activity, calcium deposition and osteogenic markers, including RUNX2 and ALP, after the overexpression of miR-424 as well as the opposite effects after the inhibition of miR-424. [score:7]
Nevertheless, we cannot completely eliminate the possibility that other validated targets of miR-424, such as cell-cycle checkpoint kinase 1 (Chk1) 24, Cdc25 25, c-Myb 43, CTNNBIP1 26, NFI-A 27, and CDX2 44, may also be involved in the proliferation or osteogenic differentiation of hASCs, which are also likely to mediate an increase in the protein expression of FOXO1 in response to miR-424 overexpression. [score:7]
At first, the transfection of the miR-424 mimic led to increased miR-424 expression at 3 days, whereas the transfection of the miR-424 inhibitor led to decreased miR-424 expression at 3 days (Fig. 3a). [score:7]
We tested whether the upregulation of FOXO1 and FGF2 resulted from the downregulation of miR-424 under oxidative stress. [score:7]
The observations that the protein expression of FGF2 was negatively regulated by miR-424 and that miR-424 has no effect on the mRNA expression of FGF2 indicate that FGF2 is regulated by miR-424 at the post-transcriptional level. [score:7]
Moreover, we found that the inhibition of FGF2 using siRNA abolished the positive effects of miR-424 knockdown on the proliferation and osteogenic differentiation of hASCs exposed to H [2]O [2], suggesting that miR-424 exerts its effects by targeting FGF2 under oxidative stress. [score:6]
Because miR-424 has been validated to target FGF2 in pulmonary artery endothelial cells using a luciferase report assay by Kim et al. in a recent study 33, we speculate that miR-424 probably targets FGF2 by binding to the 3′ untranslated region (UTR) in hASCs as well, but we did not further perform the validation. [score:6]
How to cite this article: Li, L. et al. FOXO1 -suppressed miR-424 regulates the proliferation and osteogenic differentiation of MSCs by targeting FGF2 under oxidative stress. [score:6]
Howerver, there exists a discrepancy in our study that although the expression of miR-424 was slightly downregulated, it did not significantly decrease during osteogenic differentiation. [score:6]
In addition, miR-424 expression was slightly downregulated during osteogenic differentiation, but it was not statistically significant (Fig. 3a). [score:6]
Indeed, the proliferative effect of miR-424 downregulation was abolished by FGF2 knockdown (Fig. 4f). [score:5]
The transfection of FOXO1 siRNA and the cotransfection of FOXO1 siRNA and the miR-424 inhibitor led to decreased FOXO1 expression at 3 days (Supplementary Fig. 1). [score:5]
Although both FGF2 and FOXO1 are predicted targets of miR-424, we found that miR-424 only negatively regulates FGF2, which is in turn known to be a regulator of various cell processes including proliferation and differentiation 32. [score:5]
The overexpression of miR-424 led to a significant decrease, whereas the inhibition of miR-424 led to a significant increase in the mineralization of hASCs (Fig. 3d,e). [score:5]
A chemically synthesized miRNA mimic and inhibitor (Ribobio, Guangzhou, China) were used to augment and inhibit miR-424 function, respectively. [score:5]
After seeding for 24 h, cells were transfected with 50 nM miR-424 mimic, mimic NC, 100 nM miR-424 inhibitor, and inhibitor NC or 50 nM FOXO1 siRNA, FGF2 siRNA, and NC siRNA for 24 h using the riboFECT™ CP Transfection Kit according to the manufacturer’s protocol (Ribobio, Guangzhou, China). [score:5]
To further confirm the expression of miR-424 under oxidative stress, real-time quantitative polymerase chain reaction (qRT-PCR) was performed after hASCs were incubated with 80 μM H [2]O [2] for 24 h. Compared with the control group, miR-424 was downregulated in hASCs exposed to H [2]O [2]. [score:5]
hASCs were transfected with a miR-424 mimic and a miR-424 inhibitor for 24 h. A mimic NC (negative control) and an inhibitor NC were used as a negative control. [score:5]
These factors have crucial roles in bone formation and their expression have an inverse correlation with miR-424 expression under oxidative stress. [score:5]
Recently, decreased miR-424 expression was identified in osteogenically differentiated MSCs using miRNA microarrays 6 7, suggesting that miR-424 expression is negatively correlated with osteogenic differentiation. [score:5]
Collectively, these data indicate that miR-424 inhibits the proliferation and osteogenic differentiation of hASCs by targeting FGF2 under oxidative stress. [score:5]
Furthermore, we examined whether the knockdown of FGF2 reversed the proliferative and osteogenic effects of miR-424 downregulation on hASCs under oxidative stress. [score:5]
The mRNA levels of both FOXO1 and FGF2 at 3 days were not significantly altered by the overexpression or inhibition of miR-424 in hASCs exposed to H [2]O [2] (Fig. 4a,b). [score:5]
However, the protein expression of FGF2 at 3 days was significantly decreased by treatment with the miR-424 mimic and increased by treatment with the miR-424 inhibitor based on (Fig. 4c,e). [score:5]
Our finding that the knockdown of FOXO1 completely abolished the reduction of miR-424 in hASCs exposed to H [2]O [2] suggested that FOXO1 mediates the downregulation of miR-424 under oxidative stress. [score:5]
In summary, the results obtained in this study revealed that FOXO1 -suppressed miR-424 exhibited dual effects by controlling both the proliferation and osteogenic differentiation of MSCs by targeting FGF2 under oxidative stress. [score:5]
Accordingly, we tested whether miR-424 expression is regulated by FOXO1. [score:4]
These findings support the development of new strategies of inhibiting miR-424 and augmenting FOXO1 and FGF2 to guide the modification of bone repair biomaterials and promote bone formation. [score:4]
We found that miR-424 is significantly downregulated in the porcine spine fusion and in a cell mo del of oxidative stress induced by H [2]O [2]. [score:4]
We found decreased miR-424 expression at 2 weeks compared to 4 and 8 weeks after implantation of rhBMP-2 and bone autograft in the ALIF mo del (Fig. 2a), suggesting that miR-424 expression decreased at an early stage of implantation when oxidative stress was at its peak. [score:4]
However, the inhibition was rescued, in part, by the knockdown of miR-424 (Fig. 6c,d). [score:4]
qRT-PCR showed that the knockdown of FOXO1 restored miR-424 expression in hASCs exposed to H [2]O [2] for 24 h. * P < 0.05, ns, not significant. [score:4]
The ALP activity was significantly reduced in response to miR-424 overexpression and elevated in response to miR-424 knockdown (Fig. 3c). [score:4]
Thus, it is suggested that the downregulation of miR-424 is mediated by FOXO1 in a transcriptional manner under oxidative stress. [score:4]
However, we found that the inhibition of FGF2 was sufficient to fully counter the effects of miR-424 knockdown on hASCs. [score:4]
This result suggested that FGF2 expression is regulated by FOXO1 via miR-424. [score:4]
The overexpression of miR-424 significantly reduced the proliferation of hASCs in response to H [2]O [2]. [score:3]
The expression levels of each mRNA and miR-424 were normalized to that of GAPDH and U6, respectively. [score:3]
We found that the mRNA expression of RUNX2 and ALP, two key osteogenesis markers, changed in a manner consistent with the effects of miR-424 on the ALP activity and mineralization (Fig. 3f,g). [score:3]
The mRNA expression levels of miR-424 (b), FOXO1 (c), FGF2 (d) and FOXO3 (e) were determined by qRT-PCR. [score:3]
Expression of miR-424, FOXOs, and FGF2 under oxidative stress. [score:3]
The expression of miR-424, FOXOs, and FGF2 under oxidative stress. [score:3]
To determine the roles of miR-424 in hASCs under oxidative stress, cells were transfected with a miR-424 mimic and a miR-424 inhibitor. [score:3]
In view of the negative effect of miRNAs, our data suggest that miR-424 might target FGF2, not FOXO1, under oxidative stress. [score:3]
These results suggest that miR-424 might be suppressed by FOXO1 in a transcriptional manner under oxidative stress. [score:3]
Moreover, the expression of miR-424 in human bone marrow–derived mesenchymal stem cells (hBMSCs) is higher than in osteoblasts 31. [score:3]
Simultaneously, the inhibition of miR-424 significantly promoted the proliferation of hASCs (Fig. 3b). [score:3]
Taken together, our results suggest that miR-424 inhibits the proliferation and osteogenic differentiation of hASCs under oxidative stress. [score:3]
Furthermore, the knockdown of FOXO1 led to the decreased proliferation of hASCs exposed to H [2]O [2], whereas the knockdown of miR-424, in part, abrogated the anti-proliferative effect (Fig. 6b). [score:3]
MiR-424 targets FGF2, not FOXO1, under oxidative stress. [score:2]
FOXO1 negatively regulates miR-424 in a transcriptional manner. [score:2]
MiR-424 targets FGF2, not FOXO1. [score:2]
In addition, the current study focused on the regulatory mechanism of miR-424 that links FOXO1 to FGF2 during bone formation. [score:2]
In addition, miR-424 is involved in the regulation of adipogenic differentiation of hASCs 30. [score:2]
The primers used to amplify the target mRNA and miR-424 are listed in Table 1. All experiments were performed using a real-time PCR system (CFX ConnectTM Real-time system, Bio-Rad, USA). [score:2]
To assess whether, we first determined whether FGF2 is regulated by FOXO1 via miR-424 under oxidative stress. [score:2]
MiR-424 inhibits the proliferation and osteogenic differentiation of hASCs under oxidative stress. [score:2]
In addition, the reduction was completely abrogated after the concomitant knockdown of FOXO1 and miR-424 (Fig. 6a). [score:2]
Because it has previously been reported that miR-424 targets FGF2, the corresponding validation using a dual-luciferase reporter assay was not performed in our study. [score:2]
Collectively, these findings indicate that miR-424, FOXO1, and FGF2 were simultaneously regulated by oxidative stress and that FOXO1 may be involved in maintaining redox homeostasis. [score:2]
Indeed, the knockdown of FOXO1 using siRNA completely abolished the reduction in the level of miR-424 in hASCs exposed to H [2]O [2] for 24 h (Fig. 5a). [score:2]
MiR-424 inhibits the proliferation and osteogenic differentiation of hASCs. [score:2]
In addition, FOXO1 enhances bone formation, at least partly, through the miR-424/FGF2 pathway. [score:1]
Taken together, these data suggest that FOXO1 promotes proliferation and osteogenic differentiation, at least partly, through the miR-424/FGF2 pathway under oxidative stress. [score:1]
FOXO1 promotes proliferation and osteogenic differentiation through the miR-424/FGF2 pathway under oxidative stress. [score:1]
Another limitation is that we did not evaluate other validated and potentiated targets of miR-424. [score:1]
Thus, we are cautious to extend the effects of miR-424 on in vivo bone formation and the underlying mechanism. [score:1]
Three optimal FOXO1 consensus binding sites (BS) in the promoter of miR-424 were identified according to the JASPAR database. [score:1]
Immunoprecipitation of FOXO1 with the miR-424 promoter was performed using the polyclonal mouse anti-FOXO1 antibody (ChIP grade; Abcam) and the Chromatin Immunoprecipitation Kit (EZ-ChIP™ Millipore). [score:1]
Furthermore, we found a novel mechanism in that FOXO1 promotes bone formation, at least partly, through the miR-424/FGF2 pathway. [score:1]
Three optimal FOXO1 consensus binding sites (BS) in the promoter of miR-424 were identified according to bioinformatics analysis (Fig. 5b). [score:1]
Thereafter, PCR was performed for the analysis of FOXO1 binding to the promoter of miR-424. [score:1]
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2
[+] score: 13
Under the stress of PCMV infection, 73 miRNAs were upregulated and 57 miRNAs were downregulated in porcine macrophages compared with their expression levels in the uninfected group, of which four specific upregulated miRNAs (ssc-miR-424-3p, ssc-miR-novel-chr15_16769, ssc-miR-novel-chr16_17559, ssc-miR-novel-JH118654-1_42487) were expressed only in PCMV-infected porcine macrophages. [score:13]
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3
[+] score: 7
As shown in the heat map, compared with sample on PID 0, most miRNAs were down-regulated in sample on PID 4, whereas only few miRNAs were differentially expressed in sample on PID 7. Compared with sample on PID 4, a majority of miRNAs were up-regulated in sample on PID 7. To validate the Solexa sequencing results, qRT-PCR was performed separately to investigate the relative expression levels of 5 randomly selected DE miRNAs (ssc-miR-424-3p, ssc-miR-542-5p, ssc-miR-365-5p, ssc-miR-450b-5p, ssc-miR-450a). [score:7]
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4
[+] score: 7
However, previous research reports that miR-424 regulates monocyte and macrophage differentiation [47], while miR-126 expression alters cell cycle progression of cancer cells by decreasing tumor growth and proliferation [48]. [score:4]
MiR-432 was moderately abundant during early fetal development at d 60, while miR-424 abundance increased during d 90 and d 105, and miR-126 abundance increased during later stages of fetal development at d 90 and 105. [score:3]
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5
[+] score: 4
The qRT-PCR results showed that the expression patterns of miR-204 and miR-424-5p in the PAMs of Tongcheng pigs after infection with PRRSV WUH3 are similar with those obtained from our deep sequencing data analysis (Fig. 2a, b, e and f). [score:3]
2. We randomly chose three DEmiRNAs (miR-204, miR-148a-3p, miR-424-5p) in the lung tissues of Tongcheng pigs from our data. [score:1]
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6
[+] score: 3
Three category patterns from the DEMs were clustered based on the expression percentages including early-middle embryonic stage from miR-124 to miR-424, late embryonic stage from miR-345 to miR-451 and adult stage from miR-29b to miR-133a, respectively. [score:3]
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7
[+] score: 2
1 and miR-424 regulates human monocyte/macrophage differentiation. [score:2]
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8
[+] score: 1
Many immune-related miRNAs have been identified in innate and adaptive immune systems, including the miR-17—92 cluster, miR-221, miR-10, miR-196b, miR-126, miR-155, miR-150; miR-181a, miR-326, miR-142-3p, miR-424, miR-21, miR-106a, miR-223, miR-146; the let-7 family, miR-9, and miR-34 [6]. [score:1]
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9
[+] 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-17, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26a-1, hsa-mir-27a, hsa-mir-29a, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-199a-1, hsa-mir-208a, hsa-mir-148a, hsa-mir-10a, hsa-mir-181a-2, hsa-mir-181c, hsa-mir-199a-2, hsa-mir-181a-1, hsa-mir-214, hsa-mir-221, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-23b, hsa-mir-27b, hsa-mir-125b-1, hsa-mir-128-1, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-143, hsa-mir-125b-2, hsa-mir-126, hsa-mir-127, hsa-mir-206, hsa-mir-1-1, hsa-mir-128-2, hsa-mir-29c, hsa-mir-26a-2, hsa-mir-378a, hsa-mir-148b, hsa-mir-133b, hsa-mir-424, ssc-mir-125b-2, ssc-mir-148a, ssc-mir-23a, ssc-mir-24-1, ssc-mir-26a, ssc-mir-29b-1, ssc-mir-181c, ssc-mir-214, ssc-mir-27a, ssc-let-7c, ssc-let-7f-1, ssc-let-7i, ssc-mir-103-1, ssc-mir-128-1, ssc-mir-29c, hsa-mir-486-1, hsa-mir-499a, hsa-mir-503, hsa-mir-411, hsa-mir-378d-2, hsa-mir-208b, hsa-mir-103b-1, hsa-mir-103b-2, ssc-mir-17, ssc-mir-221, ssc-mir-133a-1, ssc-mir-1, ssc-mir-503, ssc-mir-181a-1, ssc-mir-206, ssc-let-7a-1, ssc-let-7e, ssc-let-7g, ssc-mir-378-1, ssc-mir-133b, ssc-mir-29a, ssc-mir-199a-2, ssc-mir-128-2, ssc-mir-499, ssc-mir-143, ssc-mir-10a, ssc-mir-486-1, ssc-mir-103-2, ssc-mir-181a-2, ssc-mir-27b, ssc-mir-24-2, ssc-mir-23b, ssc-mir-148b, ssc-mir-208b, ssc-mir-127, ssc-mir-125b-1, hsa-mir-378b, hsa-mir-378c, ssc-mir-411, ssc-mir-133a-2, ssc-mir-126, ssc-mir-199a-1, ssc-mir-378-2, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-499b, ssc-let-7a-2, ssc-mir-486-2, hsa-mir-378j, ssc-let-7d, ssc-let-7f-2, ssc-mir-29b-2, hsa-mir-486-2, ssc-mir-378b
In addition to the best-studied myomiRs (miR-1, -206 and miR-133 families), 11 other DE muscle-related miRNAs (miR-378 [24], miR-148a [27], miR-26a [28, 29], miR-27a/b [30, 31], miR-23a [32, 33], miR-125b [34], miR-24 [35], miR-128 [36], miR-199a [37] and miR-424 [38]) with high abundance (average RPM >1,000) and another 14 (miR-181a/b/c/d-5p [26], miR-499-5p [11], miR-503 [38], miR-486 [39], miR-214 [40], miR-29a/b/c [41– 43], miR-221/222 [44] and miR-208 [11] with low abundance (average RPM <1,000) were detected in myogenesis of pig. [score:1]
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