Expression of miR-206 in Human Knee Articular Chondrocytes and Effects of miR-206 on Proliferation and Apoptosis of Articular Chondrocytes

Ni, Zhen; Shang, Xifu; Tang, Guo-Lin; Niu, Lei

doi:10.1016/j.amjms.2017.11.003

Cited by 22 publications

(15 citation statements)

References 39 publications

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“…The most significant DE miRNAs were miR-127–3 p (FC=0.5, FDR=1.1×10 −6 ) and miR-451a (FC=2.3, FDR=1.2×10 −6 ). As shown in figure 2A, the majority of DE miRNAs were upregulated in lesioned as compared with preserved OA cartilage (91 out of 142 miRNAs) with miR-206, recently reported in relation to OA,22 displaying the largest FC (FC=4.9, FDR=3.5×10 −6 ). Conversely miR-504–5 p (FC=0.4, FDR=2×10 −5 ) showed the largest fold decrease in lesioned OA cartilage (figure 2A, online supplementary table-S2).…”

Section: Resultsmentioning

confidence: 77%

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RNA sequencing data integration reveals an miRNA interactome of osteoarthritis cartilage

et al. 2018

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ObjectiveTo uncover the microRNA (miRNA) interactome of the osteoarthritis (OA) pathophysiological process in the cartilage.MethodsWe performed RNA sequencing in 130 samples (n=35 and n=30 pairs for messenger RNA (mRNA) and miRNA, respectively) on macroscopically preserved and lesioned OA cartilage from the same patient and performed differential expression (DE) analysis of miRNA and mRNAs. To build an OA-specific miRNA interactome, a prioritisation scheme was applied based on inverse Pearson’s correlations and inverse DE of miRNAs and mRNAs. Subsequently, these were filtered by those present in predicted (TargetScan/microT-CDS) and/or experimentally validated (miRTarBase/TarBase) public databases. Pathway enrichment analysis was applied to elucidate OA-related pathways likely mediated by miRNA regulatory mechanisms.ResultsWe found 142 miRNAs and 2387 mRNAs to be differentially expressed between lesioned and preserved OA articular cartilage. After applying prioritisation towards likely miRNA-mRNA targets, a regulatory network of 62 miRNAs targeting 238 mRNAs was created. Subsequent pathway enrichment analysis of these mRNAs (or genes) elucidated that genes within the ‘nervous system development’ are likely mediated by miRNA regulatory mechanisms (familywise error=8.4×10−5). Herein NTF3 encodes neurotrophin-3, which controls survival and differentiation of neurons and which is closely related to the nerve growth factor.ConclusionsBy an integrated approach of miRNA and mRNA sequencing data of OA cartilage, an OA miRNA interactome and related pathways were elucidated. Our functional data demonstrated interacting levels at which miRNA affects expression of genes in the cartilage and exemplified the complexity of functionally validating a network of genes that may be targeted by multiple miRNAs.

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Section: Resultsmentioning

confidence: 77%

“…In our DE miRNA data set, we identified many of the previously reported, OA-associated, miRNAs such as miR-20622 and miR-140 15 16. However, in our miRNA interactome, these miRNAs did not necessarily correlate to their previously reported target genes.…”

Section: Discussionmentioning

confidence: 75%

RNA sequencing data integration reveals an miRNA interactome of osteoarthritis cartilage

et al. 2018

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“…Furthermore, GIT1 was identified as a putative target of miR-206 by harboring a miR-206 binding sequence in the 3ʹ-UTR of its mRNA. A recent study [11] demonstrated that miR-206 overexpression significantly inhibited the proliferation, promoted chondrocyte apoptosis, dramatically decreased Col2a1 and aggrecan, and increased Runx2 and MMP-13 [11], indicating the involvement of miR-206 in cartilage degradation in OA. Furthermore, GIT1 has been shown to promote chondrocytes proliferation and inhibit chondrocytes apoptosis [12][13][14].…”

Section: Discussionmentioning

confidence: 99%

“…miRNAs play crucial roles in all cellular processes and also important in the process of chondrogenesis and cartilage remodeling [10]. A recent study [11] demonstrated that miR-206, which was significantly increased in human OA tissues and chondrocytes, significantly inhibited the proliferation and promoted apoptosis of chondrocytes. These data indicated that miR-206 may involve in cartilage degradation in OA and manipulation of miR-206 expression in human chondrocytes may be a novel therapeutic strategy for OA.…”

Section: Introductionmentioning

confidence: 99%

MSC-derived exosomes promote proliferation and inhibit apoptosis of chondrocytes via lncRNA-KLF3-AS1/miR-206/GIT1 axis in osteoarthritis

Liu¹,

Lin²,

Zou³

et al. 2018

Cell Cycle

251

195

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Background: Exosomes secreted by human mesenchymal stem cells (hMSCs) have been shown to promote cartilage regeneration. This study aimed to explore whether exosomal lncRNA-KLF3-AS1 derived from hMSCs can promote chondrocyte proliferation via miR-206/GIT1 axis in osteoarthritis (OA). Methods: hMSCs and MSC-derived exosomes (MSC-exo) were prepared for morphological observation and identification by transmission electron microscopy (TEM) and flow cytometry. IL-1β-induced OA chondrocytes and collagenase-induced mouse OA model were established for the further experiments. Luciferase activity assay was performed to test whether miR-206 could bind to KLF3-AS1 or GIT1. Cell proliferation and apoptosis were evaluated by CCK-8 assay and flow cytometry, respectively. Results: MSC-Exos increased chondrogenic genes Col2a1 (type II collagen alpha 1) and aggrecan, decreased hondrocyte hypertrophy markers MMP-13 (matrix metalloproteinase-13) and Runx2 (runtrelated transcription factor 2) in chondrocytes isolated from OA model mice. Furthermore, MSC-Exos attenuated IL-1β-induced chondrocyte proliferation inhibition and apoptosis induction. Moreover, MSC KLF3-AS1 -Exos (exosomes derived from KLF3-AS1-overexpressing-MSCs) ameliorated IL-1β-induced chondrocyte injury. Results also demonstrated that KLF3-AS1 acted as a competitive endogenous RNA (ceRNA) by sponging miR-206 to facilitate GIT1 expression. In addition, miR-206 overexpression and GIT1 knockdown reversed MSC KLF3-AS1 -Exos-mediated attenuation of chondrocyte injury. Conclusion: Exosomal KLF3-AS1 derived from MSCs involved in MSC-Exos-mediated chondrocyte proliferation induction and chondrocyte apoptosis inhibition via miR-206/GIT1 axis. Abbreviation: G-protein-coupled receptor kinase interacting protein-1 (GIT1) ARTICLE HISTORY

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“…The protective effects of miR-206 on inhibition of cell proliferation and promotion of cell apoptosis have also been widely studied in various human diseases including knee articular osteoarthritis, prostate cancer, cervical cancer, triple negative breast cancer and etc. [37][38][39][40]. All these findings suggest the essential roles of miR-206 in the modulation of pathophysiology of human diseases including AMI.…”

Section: Discussionmentioning

confidence: 75%

The protective role of MiR-206 in regulating cardiomyocytes apoptosis induced by ischemic injury by targeting PTP1B

et al. 2020

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MicroRNAs play essential roles in the regulation and pathophysiology of acute myocardial infarction (AMI). The purpose of the present study was to assess the expression signature of miR-206 in rat heart with AMI and the corresponding molecular mechanism. The expression of miR-206 significantly decreased in the infarcted myocardial areas and in hypoxia-induced cardiomyocytes, compared with that in the noninfarcted areas. Overexpression of miR-206 decreased cardiomyocytes apoptosis and the down-regulation of miR-206 increased cardiomyocytes apoptosis in vitro. In addition, overexpression of miR-206 in rat heart in vivo remarkably reduced myocardial infarct size and cardiomyocytes apoptosis. We identified that miR-206 had a protective effect on cardiomyocytes apoptosis with the association of its target protein tyrosine phosphatase 1B (PTP1B). Gain-of-function of miR-206 inhibited PTP1B expression and loss-of-function of miR-206 up-regulated PTP1B expression. Furthermore, overexpression of PTP1B significantly increased cardiomyocytes apoptosis. These results together suggest the protective effect of miR-206 against cardiomyocytes apoptosis induced by AMI by targeting PTP1B.

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Expression of miR-206 in Human Knee Articular Chondrocytes and Effects of miR-206 on Proliferation and Apoptosis of Articular Chondrocytes

Cited by 22 publications

References 39 publications

RNA sequencing data integration reveals an miRNA interactome of osteoarthritis cartilage

RNA sequencing data integration reveals an miRNA interactome of osteoarthritis cartilage

MSC-derived exosomes promote proliferation and inhibit apoptosis of chondrocytes via lncRNA-KLF3-AS1/miR-206/GIT1 axis in osteoarthritis

The protective role of MiR-206 in regulating cardiomyocytes apoptosis induced by ischemic injury by targeting PTP1B

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