Upregulation of microRNA‐27a inhibits synovial angiogenesis and chondrocyte apoptosis in knee osteoarthritis rats through the inhibition of PLK2

软骨细胞 血管生成 下调和上调 小RNA 骨关节炎 细胞凋亡 软骨 癌症研究 化学 医学 细胞生物学 病理 生物 解剖 生物化学 基因 替代医学
作者
Wenjing Liu,Zhuqing Zha,Haitao Wang
出处
期刊:Journal of Cellular Physiology [Wiley]
卷期号:234 (12): 22972-22984 被引量:24
标识
DOI:10.1002/jcp.28858
摘要

The function of microRNA-27a (miR-27a) on synovial angiogenesis and chondrocyte apoptosis in rats with knee osteoarthritis (KOA) by targeting PLK2 is explored in this present study. The rat model of KOA was conducted by anterior cruciate ligament transection. Rats were injected with miR-27a mimics, mimics NC, pcDNA3.1-PLK2 pcDNA3.1, or RLK2 RNAi plasmid via tail vein. A series of assays were used to figure out the functions of miR-27a and PLK2 in synovial angiogenesis and chondrocyte apoptosis in rats with KOA. Furthermore, the putative binding site between miR-27a and PLK2 was determined. Downregulated miR-27a was found in synovial tissues and cartilage tissues of KOA rats. Upregulated miR-27a and downregulated PLK2 inhibited synovial injury and promoted apoptosis of synovial cells, inhibited synovial angiogenesis, inhibited cartilage injury and chondrocyte apoptosis, inhibited cartilage collagen destruction, and alleviates inflammatory injury of synovial tissue and cartilage tissue in KOA rats. Overexpression of PLK2 reverses the effect of upregulation of miR-27a on synovial angiogenesis and chondrocyte injury in KOA rats. Our study suggests that upregulation of miR-27a inhibits synovial angiogenesis and chondrocyte apoptosis in KOA rats through the inhibition of PLK2.
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