期刊
RHEUMATOLOGY
卷 49, 期 11, 页码 2054-2060出版社
OXFORD UNIV PRESS
DOI: 10.1093/rheumatology/keq247
关键词
miRNA-34a; Chondrocyte apoptosis; miRNA-34a-specific locked nucleotide analogue; Osteoarthritis
类别
Methods. Locked nucleotide analogue (LNA)-modified miR-34a-specific anti-sense was transfected into rat chondrocyte monolayer culture. After that, IL-1 beta was added to the chondrocytes to create an OA model in vitro. The effect of silencing miR-34a on the prevention of chondrocyte apoptosis was analysed by assessment of the expression levels of Col2a1 and iNOS, also through assessment of cell viability and TUNEL staining. Results. The expression of miR-34a was significantly up-regulated by IL-1 beta. Silencing of miR-34a significantly prevented IL-1 beta-induced down-regulation of Col2a1, as well as IL-1 beta-induced up-regulation of iNOS. Finally, MiR-34a inhibitor could also reduce TUNEL-positive cells. Conclusion. Silencing of miR-34a by LNA-modified anti-sense could effectively reduce rat chondrocyte apoptosis induced by IL-1 beta. This present study revealed that silencing of miR-34a might develop a novel intervention for OA treatment through the prevention of cartilage degradation.
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