miR‑335‑5P contributes to human osteoarthritis by targeting HBP1
Xiaokun Lu, Yu Li, Huimin Chen, Yuancheng Pan, Ran Lin, Shunyou Chen
Abstract
MicroRNA (miR)‑335‑5P has the ability to regulate chondrogenic differentiation and promote chondrogenesis in mouse mesenchymal stem cells. It is also abnormally elevated in human osteoarthritic chondrocytes. However, the biological function of miR‑335‑5P in osteoarthritis (OA) is not well understood. The present study investigated the mechanism of miR‑335‑5P in the pathogenesis of OA. To investigate the effect of miR‑335‑5P on the pathogenesis of OA <em>in vitro</em>, a miR‑335‑5P mimic and inhibitor were transfected into chondrocytes. Cell Counting kit‑8 assay and flow cytometry were used to observe the effects of miR‑335‑5P on chondrocyte apoptosis and the expression of cartilage‑specific genes, such as aggrecan, collagen II, matrix metalloproteinase 13 and collagen X, were detected by reverse transcription‑quantitative PCR and western blot analysis. Moreover, the current study assessed whether HMG‑box transcription factor 1 (HBP1) is a novel target of miR‑335‑5P with dual luciferase reporter assays. Finally, a rescue experiment was used to prove the regulation between miR‑335‑5P and HBP1. The results revealed that HBP1 was a novel target of miR‑335‑5P, and that miR‑335‑5P mediated the apoptosis of chondrocytes and changes in cartilage‑specific genes via targeting HBP1. Overall, the present study revealed that miR‑335‑5P mediated the development of OA by targeting the HBP1 gene and promoting chondrocyte apoptosis. These data suggested that miR‑335‑5P may be used to develop novel early‑stage diagnostic and therapeutic strategies for OA.