Osteoarthritis (OA) is a common joint disease characterized by degradation of the articular cartilage and joint inflammation. Studies have revealed the importance of microRNAs in the regulation of chondrocyte apoptosis. MicroRNA deep sequencing of control and osteoarthritic cartilage has revealed that miR-10a-5p is significantly upregulated in osteoarthritic tissues. However, its role in these tissues remains unknown. The present study was conducted to investigate the effect of miR-10a-5p in promoting OA. miR-10a-5p expression was increased in chondrocytes after interleukin-1β treatment in vitro. Transfection with a miR-10a-5p inhibitor abrogated interleukin-1β-induced apoptosis. A luciferase activity assay showed that miR-10a-5p targeted the 3′ UTR of the homeobox gene HOXA1, inhibiting its expression. Treatment with HOXA1 siRNA reversed the rescuing effect of the miR-10a-5p inhibitor on chondrocyte apoptosis. Additionally, an OA model was established in mice by anterior cruciate ligament transection. AntagomiR-10a-5p improved the cartilage surfaces of osteoarthritic mice, whereas agomiR-10a-5p worsened them. A terminal deoxynucleotidyl transferase dUTP nick-end labeling assay indicated reduced apoptosis and increased HOXA1 expression in osteoarthritic mice after miR-10a-5p knockdown. These findings reveal a novel mechanism regulating OA progression and demonstrate the potential of miR-10a-5p and homeobox protein HOXA1 as therapeutic targets.

骨关节炎（OA）是一种常见的关节疾病，其特征是关节软骨退化和关节发炎。研究表明微RNA在调节软骨细胞凋亡中的重要性。对照和骨关节炎软骨的MicroRNA深度测序显示，miR-10a-5p在骨关节炎组织中显着上调。然而，其在这些组织中的作用仍然未知。进行本研究以研究miR-10a-5p在促进OA中的作用。白细胞介素1β体外培养后，软骨细胞中miR-10a-5p表达增加。用miR-10a-5p抑制剂转染可消除白介素-1β诱导的细胞凋亡。荧光素酶活性测定表明miR-10a-5p靶向同源盒基因HOXA1的3'UTR，抑制其表达。HOXA1 siRNA处理逆转了miR-10a-5p抑制剂对软骨细胞凋亡的挽救作用。另外，通过前交叉韧带横断在小鼠中建立了OA模型。AntagomiR-10a-5p改善了骨关节炎小鼠的软骨表面，而agomiR-10a-5p使它们恶化。终端脱氧核苷酸转移酶dUTP缺口末端标记试验表明，miR-10a-5p敲除后，骨关节炎小鼠的凋亡减少，HOXA1表达增加。这些发现揭示了调节OA进程的新机制，并证明了miR-10a-5p和同源盒蛋白HOXA1作为治疗靶标的潜力。