Department of Orthopedics, the Fourth Affiliated Hospital of China Medical University, No.4 East Chongshan Road, Shenyang, 110032, P.R. China.
Center for Translational Medicine, the Fourth Affiliated Hospital of China Medical University, No.4 East Chongshan Road, Shenyang, 110032, P.R. China.
Int J Med Sci. 2021 Jan 1;18(4):902-910. doi: 10.7150/ijms.50984. eCollection 2021.
The pathogenesis of hallux valgus is not clearly understood. However, genetics research about hallux valgus is rare. Therefore, the present study aimed to explore the pathogeny of hallux valgus from the perspective of genetics. Human samples were collected from normal bone tissue and hallux valgus region bone tissue. The bone samples were studied using real time-PCR, western blot and immunohistochemical. Lentivirus-mediated miR-182 transfected osteoblasts and tested the expression of FGF9 mRNA with real time-PCR. To test alkaline phosphatase activity, number of calcium nodules and proliferation of osteoblast with enzymatic activity analysis, calcium nodules stained and MTT assay. We found that (1) FGF9 expressed in hallux valgus region bone tissue was significantly higher than normal bone tissue. (2) miR-182 expression levels in hallux valgus region bone tissue were notably lower than those of normal bone tissue. (3) miR-182 could negatively regulate the expression of FGF9 in osteoblasts. (4) FGF9 may enhance osteoblasts proliferation. We have demonstrated that miR-182 promotes the formation of bone by targeting FGF9, implicating an essential role of miR-182 in the etiology of hallux valgus. Moreover, miR-182 might potentially be a therapeutic target for hallux valgus treatment.
拇外翻的发病机制尚不清楚。然而，关于拇外翻的遗传学研究很少。因此，本研究旨在从遗传学的角度探讨拇外翻的发病机制。从正常骨组织和拇外翻区骨组织中采集人样本。使用实时 PCR、western blot 和免疫组织化学研究骨样本。用慢病毒介导的 miR-182 转染成骨细胞，并通过实时 PCR 检测 FGF9 mRNA 的表达。通过酶活性分析检测碱性磷酸酶活性、钙结节数量和成骨细胞增殖，用钙结节染色和 MTT 测定。我们发现：（1）拇外翻区骨组织中 FGF9 的表达明显高于正常骨组织。（2）拇外翻区骨组织中 miR-182 的表达水平明显低于正常骨组织。（3）miR-182 可负向调节成骨细胞中 FGF9 的表达。（4）FGF9 可能增强成骨细胞的增殖。我们已经证明，miR-182 通过靶向 FGF9 促进骨形成，表明 miR-182 在拇外翻的发病机制中起重要作用。此外，miR-182 可能是治疗拇外翻的潜在靶点。
