International journal of rheumatic diseases · 2026
The Clinical Role of miR-744-5p in Osteoarthritis and Its Regulation of Chondrocyte Inflammation Through the Modulation of Thrombospondin-2 (THBS2) Expression.
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Du Baoping, Hao Yao, Lu Hao, Wang Renwei, Xu Zhihui, Hao Weidong, Shi Fan, Wang Wenge, Li Shichen, Wang Yuhong, Li Simin
Аннотация
AIM: Osteoarthritis (OA) is a common degenerative joint disease that is difficult to diagnose in its early stages, which can easily delay treatment. MicroRNAs (miRNAs) are key regulatory factors in the pathogenesis of OA. This study investigated the clinical diagnostic value of miR-744-5p in OA and its regulatory effect on chondrocyte inflammation through modulation of thrombospondin-2 (THBS2).
METHODS: This study included 108 OA patients and 62 healthy controls. Serum levels of miR-744-5p were detected using qRT-PCR. The diagnostic value of miR-744-5p was evaluated using the ROC curve and logistic regression. LPS-induced chondrocyte OA models were used to assess the regulatory effect of miR-744-5p on chondrocyte inflammation via CCK-8 and ELISA. Dual-luciferase assay verified the targeting relationship between miR-744-5p and THBS2.
RESULTS: The serum level of miR-744-5p in OA patients was markedly reduced (p < 0.001), showing good diagnostic performance (AUC = 0.860). Logistic regression indicated that it could serve as an independent protective factor for OA (OR = 0.089). miR-744-5p mimic significantly restored the viability of chondrocytes induced by LPS (p < 0.001), inhibited the expression of inflammatory factors (p < 0.001), and alleviated oxidative stress damage. Dual-luciferase reporter assay confirmed that miR-744-5p directly targets THBS2. Overexpression of THBS2 reversed the protective effects of miR-744-5p.
CONCLUSION: miR-744-5p is significantly downregulated in OA and is a highly promising diagnostic and predictive molecule for OA. It can alleviate inflammation in chondrocytes by targeting THBS2, thereby inhibiting the progression of OA.
METHODS: This study included 108 OA patients and 62 healthy controls. Serum levels of miR-744-5p were detected using qRT-PCR. The diagnostic value of miR-744-5p was evaluated using the ROC curve and logistic regression. LPS-induced chondrocyte OA models were used to assess the regulatory effect of miR-744-5p on chondrocyte inflammation via CCK-8 and ELISA. Dual-luciferase assay verified the targeting relationship between miR-744-5p and THBS2.
RESULTS: The serum level of miR-744-5p in OA patients was markedly reduced (p < 0.001), showing good diagnostic performance (AUC = 0.860). Logistic regression indicated that it could serve as an independent protective factor for OA (OR = 0.089). miR-744-5p mimic significantly restored the viability of chondrocytes induced by LPS (p < 0.001), inhibited the expression of inflammatory factors (p < 0.001), and alleviated oxidative stress damage. Dual-luciferase reporter assay confirmed that miR-744-5p directly targets THBS2. Overexpression of THBS2 reversed the protective effects of miR-744-5p.
CONCLUSION: miR-744-5p is significantly downregulated in OA and is a highly promising diagnostic and predictive molecule for OA. It can alleviate inflammation in chondrocytes by targeting THBS2, thereby inhibiting the progression of OA.