miR-10a-5p Promotes Chondrocyte Apoptosis in Osteoarthritis by Targeting HOXA1

Ma, Yan; Wu, Yizheng; Chen, Junxin; Huang, Kai; Ji, Bin; Chen, Zhijun; Wang, Qiang; Ma, Jianjun; Shen, Shuying; Zhang, Jianfeng

doi:10.1016/j.omtn.2018.12.012

Cited by 54 publications

(43 citation statements)

References 31 publications

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“…Several miRNAs have been proven to regulate various signaling pathways, apoptosis and chondrocyte functions in OA (28). Some miRNAs are differentially expressed during the onset and development of OA (29)(30)(31). A total of 42 circRNAs have also been found to be differentially expressed in OA (32).…”

Section: Discussionmentioning

confidence: 99%

Circular RNA CSNK1G1 promotes the progression of osteoarthritis by targeting the miR‑4428/FUT2 axis

Xiao¹,

Wang

Zhou

et al. 2020

Int J Mol Med

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Osteoarthritis (OA) is a chronic disease that results in chronic arthralgia and functional disability of the affected joint. To date, there is no effective treatment available for this disease. Circular RNAs (circRNAs) are a type of intracellular stable RNA that can regulate the development and progression of OA. However, the function of circCSNK1G1 in OA has not yet been investigated. In the present study, it was found that circCSNK1G1 was upregulated in OA cartilage tissues. The upregulation of circCSNK1G1 was associated with extracellular matrix (ECM) degradation and chondrocyte apoptosis. Moreover, the expression of miR-4428 was downregulated and that of fucosyltransferase 2 (FUT2) was upregulated in OA-affected cartilage tissues. Dual-luciferase reporter assay and RNA immunoprecipitation confirmed that miR-4428 targeted FUT2 mRNA to inhibit FUT2 expression. circCSNK1G1 and FUT2 induced ECM degradation and chondrocyte apoptosis. The negative effects of circCSNK1G1 and FUT2 were reversed by miR-4428. On the whole, the present study demonstrates that circCSNK1G1 promotes the development of OA by targeting the miR-4428/FUT2 axis. Thus, the circCSNK1G1/miR-4428/FUT2 axis may present a novel target for the treatment of OA in the clinical setting.

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Section: Discussionmentioning

confidence: 99%

Circular RNA CSNK1G1 promotes the progression of osteoarthritis by targeting the miR‑4428/FUT2 axis

Xiao¹,

Wang

Zhou

et al. 2020

Int J Mol Med

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“…mirna (mir)-26a was reported to suppress the activation of the nF-κB signaling pathway to alleviate synovial inflammation and cartilage injury in oa rats (16). mir-10a-5p promoted chondrocyte apoptosis in oa by targeting homeobox a1 (17). mir-93 targets Toll-like receptor 4/nF-κB signaling to inhibit OA-associated inflammation and chondrocyte apoptosis (18).…”

Section: Introductionmentioning

confidence: 99%

Identification of microRNA‑363‑3p as an essential regulator of chondrocyte apoptosis in osteoarthritis by targeting NRF1 through the p53‑signaling pathway

Zhang

Wang

et al. 2020

Mol Med Report

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osteoarthritis (oa) is a degenerative joint disease that affects the physical, and mental health of middle-aged and elderly people. The aims of the present study were to determine the biological function and molecular mechanisms of mir-363-3p in chondrocyte apoptosis. exploration of the molecular mechanisms of oa may be helpful in the understand of the causes, and facilitating the prevention and treatment of oa. in the present study, the expression of nuclear respiratory factor1 (nrF1) was downregulated in the articular cartilage of oa rats in vivo and lipopolysaccharide (lPS)-treated chondrocytes in vitro. Micrornas (mirna) are regulators of gene expression in the progression of oa. TargetScan software was used to predict that nrF1 was a potential target for mirna (miR)-363, and this was confirmed in subsequent experiments. The expression of mir-363-3p was negatively correlated with the expression of NRF1, and its expression was significantly upregulated in oa model rats and in lPS-induced chondrocytes compared with the expression in the respective controls. in addition, the overexpression of mir-363-3p increased the levels of interleukin (il)-1β, il-6 and tumor necrosis factor-α in vivo, and was demonstrated to promote chondrocyte injury and apoptosis by Safranin o staining and Tunel. Moreover, the inhibition of mir-363-3p expression increased the expression of nrF1 and protected chondrocytes from apoptosis in vitro and in vivo, whereas the overexpression of mir-363-3p downregulated nrF1 expression and promoted lPS-induced chondrocyte apoptosis through the p53 pathway in vitro. The results of this study suggested that mir-363-3p-mediated inhibition of nrF1may be associated with chondrocyte apoptosis in oa.

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“…For example, miR‐10a‐5p, miR‐126, miR‐181a‐5, and miR‐320a can induce chondrocyte apoptosis in a model of IL‐1β‐induced OA. MiR‐10a‐5p has been reported that upregulated and induced apoptosis through repression of HOXA1 in chondrocytes (Ma et al, ). In IL‐1β‐induced cell line CHON‐001, expression of IL‐6, IL‐8, and tumour necrosis factor‐α (TNF‐α) were all increased as well as miR‐126 was upregulated, while inhibition of mir‐126 reduced apoptosis and upregulated bcl‐2 expression through inactivating MAKP/JNK signaling pathway (Yu et al, ).…”

Section: Chondrocyte Injuriesmentioning

confidence: 99%

Noncoding RNAs: New regulatory code in chondrocyte apoptosis and autophagy

Jiang

Liu

et al. 2020

WIREs RNA

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Osteoarthritis (OA) is a bone and joint disease characterized by progressive cartilage degradation. In the face of global trends of population aging, OA is expected to become the fourth most common disabling disease by 2020. Nevertheless, the detailed pathogenesis of OA has not yet been elucidated. Noncoding RNAs (ncRNAs), including long noncoding RNAs, microRNAs, and circular RNAs, do not encode proteins but have recently emerged as important regulators of apoptosis and autophagy of chondrocytes, thereby highlighting a potential role in chondrocyte injury leading to OA onset and progression. We here review recent findings on these regulatory roles of ncRNAs to provide new directions for research on the pathogenesis of OA and offer new therapeutic targets for prevention and treatment. This article is categorized under: RNA in Disease and Development > RNA in Disease RNA in Disease and Development > RNA in Development

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miR-10a-5p Promotes Chondrocyte Apoptosis in Osteoarthritis by Targeting HOXA1

Cited by 54 publications

References 31 publications

Circular RNA CSNK1G1 promotes the progression of osteoarthritis by targeting the miR‑4428/FUT2 axis

Circular RNA CSNK1G1 promotes the progression of osteoarthritis by targeting the miR‑4428/FUT2 axis

Identification of microRNA‑363‑3p as an essential regulator of chondrocyte apoptosis in osteoarthritis by targeting NRF1 through the p53‑signaling pathway

Noncoding RNAs: New regulatory code in chondrocyte apoptosis and autophagy

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