MiR-210 inhibits NF-κB signaling pathway by targeting DR6 in osteoarthritis

Zhang, Dawei; Cao, Xiaohong; Li, Jun; Zhao, Guisen

doi:10.1038/srep12775

Cited by 97 publications

(81 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In contrast to the above results, our data indicated that suppression of miR-302b suppressed LPS-induced injury of the chondrocyte cells. Our study found that knockdown of miR-302b exerts a protective role in human OA chondrocytes, which was in line with a previous study [25]. …”

Section: Discussionsupporting

confidence: 81%

Knockdown MiR-302b Alleviates LPS-Induced Injury by Targeting Smad3 in C28/I2 Chondrocytic Cells

Wang

Jin

et al. 2018

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: Osteoarthritis (OA) is one of the most common chronic degenerative diseases. Many studies have demonstrated the role of microRNAs (miRNAs) in OA; however, the role of miR-302b in OA remains elusive. The aim of this study was to identify the role of miR-302b in LPS-induced injury in chondrocytes. Methods: Human OA chondrocytes (C28/12 cell line) were transfected with miR-302b inhibitor and miR-302b mimic to investigate the effects of miR-302b expression on chondrocyte apoptosis and inflammation, and to identify the miR-302b target proteins. Results: LPS treatment of chondrocytes significantly reduced cell viability and increased apoptotic rate. LPS treatment also increased the expression of inflammatory cytokines compared to control. miR-302b was up-regulated in LPS-induced chondrocytes. miR-302b was either suppressed or overexpressed in LPS-induced chondrocytes by transient transfection. miR-302b mimic transfection accelerated the effects of LPS on cell viability, apoptosis and inflammation. Of contrast, miR-302b inhibition represented a reverse effect. Dual luciferase activity demonstrated that Smad3 is a direct target for miR-302b and its expression was negatively regulated by miR-302b. In addition, miR-302b inhibition suppressed inflammation in LPS treated chondrocytes by up-regulating Smad3 expression. Moreover, LPS induced down-regulation of Notch and mTOR signaling pathway-related protein expressions, and miR-302b inhibition increased the expressions of Notch and mTOR signaling pathway-related proteins. We further found that miR-302b negatively regulated Notch2 levels through direct targeting its 3’UTR. Conclusions: These results suggest that miR-302b suppression may function as a protector in suppressing the inflammation during the development and progression of OA by up-regulating the target Smad3 expression.

show abstract

Section: Discussionsupporting

confidence: 81%

Knockdown MiR-302b Alleviates LPS-Induced Injury by Targeting Smad3 in C28/I2 Chondrocytic Cells

Wang

Jin

et al. 2018

Cell Physiol Biochem

View full text Add to dashboard Cite

show abstract

“…Another study by Zhang et al utilized both in vitro and in vivo approaches to show potential chondroprotective effects of miR-210 (158). Overexpression of miR-210 via mimics was found to inhibit lipopolysaccharide-induced proinflammatory cytokines and cell death in primary rat chondrocytes and that one of its potential targets was death receptor 6 (DR6) mRNA.…”

Section: Other Mirnas Associated With Inflammatory Pathways In Oamentioning

confidence: 99%

Inflammation and epigenetic regulation in osteoarthritis

Shen

Abu‐Amer

O’Keefe

et al. 2016

Connective Tissue Research

185

140

View full text Add to dashboard Cite

Osteoarthritis (OA) was once defined as a non-inflammatory arthropathy, but it is now well-recognized that there is a major inflammatory component to this disease. In addition to synovial cells, articular chondrocytes and other cells of diarthrodial joints are also known to express inflammatory mediators. It has been proposed that targeting inflammation pathways could be a promising strategy to treat OA. There have been many reports of cross-talk between inflammation and epigenetic factors in cartilage. Specifically, inflammatory mediators have been shown to regulate levels of enzymes that catalyze changes in DNA methylation and histone structure, as well as alter levels of non-coding RNAs. In addition, expression levels of a number of these epigenetic factors have been shown to be altered in OA, thereby suggesting potential interplay between inflammation and epigenetics in this disease. This review provides information on inflammatory pathways in arthritis and summarizes published research on how epigenetic regulators are affected by inflammation in chondrocytes. Furthermore, we discuss data showing how altered expression of some of these epigenetic factors can induce either catabolic or anti-catabolic effects in response to inflammatory signals. A better understanding of how inflammation affects epigenetic factors in OA may provide us with novel therapeutic strategies to treat this condition.

show abstract

“…Members of the TNF receptor superfamily (TNFRSF) upon activation are important inducers of apoptosis [135]. Previous studies have shown that death receptor 6 (TNFRSF21) is upregulated in OA and is targeted by miR-210, which is downregulated in OA [136, 137]. Hypoxia inducible factor-1-α (HIF-1α) regulates chondrogenesis as well as apoptosis and autophagy in chondrocytes [138].…”

Section: Mirna Regulation Of Apoptosis and Autophagy In Oamentioning

confidence: 99%

The Role of MicroRNAs and Their Targets in Osteoarthritis

2016

View full text Add to dashboard Cite

MicroRNA regulation and expression has become an emerging field in determining the mechanisms regulating a variety of inflammation-mediated diseases. Recent studies have focused on specific microRNAs that are differentially expressed in case of osteoarthritis. Furthermore, several targets of these miRNAs important in disease progression have also been identified. In this review, we focus on microRNA biogenesis, regulation, detection, and quantification with an emphasis on cellular localization and how these concepts may be linked to disease processes such as osteoarthritis. Next, we review the relationship of specific microRNAs to certain features and risk factors associated with osteoarthritis such as inflammation, obesity, autophagy, and cartilage homeostasis. We also identify selected microRNAs that are differentially expressed in osteoarthritic tissue, but have unidentified targets and functions in the disease pathogenesis. Lastly, we highlight the potential use of microRNAs for therapeutic purposes, and also point to certain remedies that regulate microRNA expression.

show abstract

MiR-210 inhibits NF-κB signaling pathway by targeting DR6 in osteoarthritis

Cited by 97 publications

References 30 publications

Knockdown MiR-302b Alleviates LPS-Induced Injury by Targeting Smad3 in C28/I2 Chondrocytic Cells

Knockdown MiR-302b Alleviates LPS-Induced Injury by Targeting Smad3 in C28/I2 Chondrocytic Cells

Inflammation and epigenetic regulation in osteoarthritis

The Role of MicroRNAs and Their Targets in Osteoarthritis

Contact Info

Product

Resources

About