Inhibition of miR-126 protects chondrocytes from IL-1β induced inflammation via upregulation of Bcl-2

Yu, Chun-Hong; Miao, Wujun; Zhang, Y. Y.; Zou, Min; Yan, Xin

doi:10.1302/2046-3758.76.bjr-2017-0138.r1

Cited by 35 publications

(26 citation statements)

References 31 publications

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“…TNF-α and IL-1β have been used to trigger inflammation in chondrocyte and synoviocyte culture. Upon stimulation, the cells release IL-6 [26], IL-8 [27], IL-10 [28], IL-1β [29], and TNF-α [28]. Similar cytokine profile was increased in animal models of osteoarthritis [18,[30][31][32][33][34].…”

Section: The Role Of Cytokines In Osteoarthritismentioning

confidence: 99%

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The Role of Inflammation in the Pathogenesis of Osteoarthritis

Chow

Chin

2020

Mediators of Inflammation

338

221

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A joint is the point of connection between two bones in our body. Inflammation of the joint leads to several diseases, including osteoarthritis, which is the concern of this review. Osteoarthritis is a common chronic debilitating joint disease mainly affecting the elderly. Several studies showed that inflammation triggered by factors like biomechanical stress is involved in the development of osteoarthritis. This stimulates the release of early-stage inflammatory cytokines like interleukin-1 beta (IL-1β), which in turn induces the activation of signaling pathways, such as nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), phosphoinositide 3-kinase/protein kinase B (PI3K/AKT), and mitogen-activated protein kinase (MAPK). These events, in turn, generate more inflammatory molecules. Subsequently, collagenase like matrix metalloproteinases-13 (MMP-13) will degrade the extracellular matrix. As a result, anatomical and physiological functions of the joint are altered. This review is aimed at summarizing the previous studies highlighting the involvement of inflammation in the pathogenesis of osteoarthritis.

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Section: The Role Of Cytokines In Osteoarthritismentioning

confidence: 99%

“…Laboratory studies showed that miR-146a [29] and miR-126 [27] were upregulated in chondrocytes induced with inflammation with lipopolysaccharide (LPS) and IL-1β, respectively. miR-146a targets CXCR4 and downregulated its expression.…”

Section: The Role Of Mirna In Osteoarthritismentioning

confidence: 99%

The Role of Inflammation in the Pathogenesis of Osteoarthritis

Chow

Chin

2020

Mediators of Inflammation

338

221

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“…Previous studies determined that chondrocyte survival was associated with joint destruction in OA patients [21,22]. The human chondrocyte cell line CHON-001, derived from normal human articular cartilage, has been widely used in vitro in osteoarthritis models [23][24][25]. Although researches have been conducted on different aspects of OA, further studies are required to be carried out on the molecular mechanisms involved in chondrocyte survival in OA.…”

Section: Discussionmentioning

confidence: 99%

LncRNA DNM3OS promotes proliferation and inhibits apoptosis through modulating IGF1 expression by sponging MiR-126 in CHON-001 cells

2019

Diagn Pathol

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Background: As a degenerative disease, osteoarthritis (OA) greatly affects aged population. The human chondrocyte cell line CHON-001, derived from normal human articular cartilage, has been widely used in vitro in osteoarthritis models. In order to better understand the underlying mechanism of OA pathogenesis, this study was conducted to explore the effects of LncRNA dynamin 3 opposite strand (DNM3OS) on CHON-001 cells. Methods: The expression levels of and correlation between DNM3OS and miR-126 that derived from OA and non-OA tissues were determined by quantitative real time (qRT)-PCR and Spearman's correlation analysis. Cell viability, clone, migration, invasion and apoptosis were respectively determined by cell counting kit-8, colony formation, wound healing assay, transwell and flow cytometry. The target genes were predicted by starbase V2 and targetscan 7.2 and confirmed by luciferase reporter assay. The expressions of apoptosis-related factors were detected by Western blot. Results: The expression of DNM3OS was down-regulated in OA patients. Functional assays demonstrated that ectopic expression of DNM3OS promoted the proliferation and inhibited apoptosis of CHON-001 cells, and that knocking down DNM3OS suppressed cell proliferation and induced apoptosis. Mechanistic investigation revealed that DNM3OS physically bound to the promoter of miR-126 and suppressed miR-126 expression. Decreased expression of DNM3OS was negatively correlated with miR-126 in OA patients. Furthermore, the effects of siDNM3OS on inhibiting cell proliferation and promoting apoptosis were partially reversed by miR-126 inhibitor. Meanwhile, type insulin-like growth factor-1 (IGF1) was identified as a target gene for miR-126 and was negatively associated with the miR-126 expression. Overexpressed IGF1 restored the effects of miR-126 mimic in suppressing cell proliferation and promoting apoptosis. Conclusion: Our results showed that DNM3OS could affect the CHON-001 cell proliferation and apoptosis by regulating IGF1 by sponging miR-126.

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“…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, ). The expression of miR‐181a‐5p was negatively correlated with selenocysteine insertion sequence elenent (SECIS)‐binding protein 2 (SBP2), GPX1 and GPX4 mRNA expression and SBP2 protein expression in the damaged cartilage were lower than normal cartilage, whereas miR‐181a‐5p expression on the contrary (Xue 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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Inhibition of miR-126 protects chondrocytes from IL-1β induced inflammation via upregulation of Bcl-2

Cited by 35 publications

References 31 publications

The Role of Inflammation in the Pathogenesis of Osteoarthritis

The Role of Inflammation in the Pathogenesis of Osteoarthritis

LncRNA DNM3OS promotes proliferation and inhibits apoptosis through modulating IGF1 expression by sponging MiR-126 in CHON-001 cells

Noncoding RNAs: New regulatory code in chondrocyte apoptosis and autophagy

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