Upregulation of microRNA‐9‐5p inhibits apoptosis of chondrocytes through downregulating Tnc in mice with osteoarthritis following tibial plateau fracture

下调和上调 小RNA 骨关节炎 细胞凋亡 高原(数学) 胫骨平台骨折 细胞生物学 医学 癌症研究 化学 生物 病理 解剖 基因 生物化学 数学分析 数学 内固定 替代医学
作者
Hongwei Chen,Jun Yang,Zhihong Tan
出处
期刊:Journal of Cellular Physiology [Wiley]
卷期号:234 (12): 23326-23336 被引量:24
标识
DOI:10.1002/jcp.28900
摘要

Osteoarthritis (OA) is a common degenerative joint disease which is typically progressed with age, affecting smaller joints of hands, lower limbs, and the vertebral column. It has been reported that microRNAs could regulate the biological processes of OA. Therefore, the purpose of this study was to elucidate miR-9-5p's role in regulating cartilage remodeling of OA mice following tibial plateau fracture (TPF) through regulation of tenascin C (Tnc). Initially, we determined the expression of miR-9-5p and Tnc in mice with OA and then testified their relationship. The results displayed a high expression of Tnc, but a poor expression of miR-9-5p with high methylation in OA. Tnc was confirmed to be a target gene of miR-9-5p. Moreover, based on gain- and loss-function experiments, an increase of miR-9-5p and loss of Tnc had the potential to inhibit cell apoptosis, while facilitating cell proliferation, migration, invasion, and cartilage remodeling of mice with OA following TPF. This was further demonstrated by a higher expression of type II collagen, lower type X collagen, and protogenin expression. Subsequently, downregulation of miR-9-5p aggravated the pathological changes of mice, illustrated by an increase in the Mankin score. In conclusion, the present study proved that overexpression of miR-9-5p suppressed chondrocytes apoptosis and promoted cartilage remodeling through downregulating of Tnc in mice with OA.
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