期刊
JOURNAL OF BONE AND MINERAL METABOLISM
卷 40, 期 3, 页码 415-421出版社
SPRINGER JAPAN KK
DOI: 10.1007/s00774-022-01310-0
关键词
Osteoarthritis; circTMOD3; miR-27a; Chondrocytes; Apoptosis
This study found that the interaction between circTMOD3 and miR-27a plays an important role in LPS-induced chondrocyte apoptosis in OA. circTMOD3 promotes chondrocyte apoptosis induced by LPS by suppressing miR-27a maturation.
Introduction The progression of osteoarthritis (OA) requires the involvement of lipopolysaccharide (LPS)-induced inflammation, in which circTMOD3 plays an important role. We predicted that circTMOD3 could interact with miR-27a to inhibit LPS-induced chondrocyte apoptosis and explored the interaction between circTMOD3 and miR-27a in OA. Materials and methods Total RNAs were isolated from cartilage tissue samples from both OA patients (n = 62) and controls (n = 62) and subjected to RT-qPCRs to determine circTMOD3 and miR-27a (mature and premature) expression. Subcellular location of circTMOD3 and its interaction with premature miR-27a were analyzed using subcellular fractionation assay and RNA-RNA pulldown assay, respectively. CircTMOD3 was overexpressed in chondrocytes to study its role in miR-27a maturation. The roles of circTMOD3 and miR-27a in LPS-induced chondrocyte apoptosis were analyzed using cell apoptosis assay. Results CircTMOD3 and premature miR-27a levels were increased while mature miR-27a level was decreased in OA. CircTMOD3 was located in both nuclear and cytoplasm fractions of chondrocytes. CircTMOD3 directly interacted with premature miR-27a and promoted LPS-induced chondrocyte apoptosis, while miR-27a inhibited LPS-induced chondrocyte apoptosis. Moreover, circTMOD3 overexpression suppressed miR-27a maturation and reduced the inhibitory effects of miR-27a on LPS-induced chondrocyte apoptosis. Conclusion CircTMOD3 suppresses miR-27a maturation in OA to promote chondrocyte apoptosis induced by LPS.
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