科研之友
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摘要
The aim of this study was to investigate the expression of miR-211-5p in osteoarthritis (OA) and to explore potential molecular mechanisms for the same. qRT-PCR was used to detect the expression of miR-211-5p in IL-1 beta-stimulated chondrocytes. Subsequent to cell transfection, the impact of the miR-211-5p mimic on viability, apoptosis, and migration of chondrocytes was determined using the Cell Counting Kit-8, flow cytometry, and the Transwell assay, respectively. Additionally, the expression profiles of Bcl-2, Bax, cleaved Caspase-3, and pro-Caspase-3 were also determined by qRT-PCR and western blot. The target gene of miR-211-5p was predicted and validated using the luciferase reporter assay. The changes in the expression levels of the NF-kappa B pathway proteins after cell transfection were detected by the western blot. The expression of miR-211-5p was observed to be down-regulated in IL-1 beta-stimulated chondrocytes. An overexpression of miR-211-5p was seen to promote chondrocytes viability, inhibit apoptosis, and increase the migratory capability of the chondrocytes. ADAMTS5 was identified as a target gene for miR-211-5p and it was determined that miR-211-5p is a negative regulator for the same. It was also determined that the impact of miR-211-5p on chondrocyte viability, apoptosis, and migration is mediated through the regulation of ADAMTS5 expression and the suppression of the NF-kappa B pathway. Our study demonstrates that miR-211-5p plays an important role in the pathogenesis of OA. The overexpression of miR-211-5p promotes viability and migration while inhibiting apoptosis of chondrocytes by negatively regulating the expression of ADAMTS5 and suppressing the NF-kappa B pathway.
- 出版日期2017
- 单位湖州市中心医院; 浙江大学
