期刊
BIOMED RESEARCH INTERNATIONAL
卷 2017, 期 -, 页码 -出版社
HINDAWI LTD
DOI: 10.1155/2017/9792512
关键词
-
资金
- Fondation pour la Recherche Medicale (FRM)
- PRST IMTS of Region Lorraine
- Communaute Urbaine du Grand Nancy (CUGN)
- CNRS
- Lorraine University
Objective. Decreased expression of collagen type II in favour of collagen type I or X is one hallmark of chondrocyte phenotype changes in osteoarthritic (OA) cartilage. MicroRNA- (miR-) 29b was previously shown to target collagens in several tissues. We studied whether it could contribute to collagen imbalance in chondrocytes with an impaired phenotype. Methods. After preliminary microarrays screening, miR-29b levels were measured by RT-quantitative PCR in in vitro models of chondrocyte phenotype changes (IL-1 beta challenge or serial subculturing) and in chondrocytes from OA and non-OA patients. Potential miR-29b targets identified in silico in 3' -UTRs of collagens mRNAs were tested with luciferase reporter assays. The impact of premiR-29b overexpression in ATDC5 cells was studied on collagen mRNA levels and synthesis (Sirius red staining) during chondrogenesis. Results. MiR-29b level increased significantly in IL-1 beta-stimulated and weakly in subcultured chondrocytes. A 5.8-fold increase was observed in chondrocytes from OA versus non-OA patients. Reporter assays showed that miR-29b targeted COL2A1 and COL1A2 3'-UTRs although with a variable recovery upon mutation. In ATDC5 cells overexpressing premiR-29b, collagen production was reduced while mRNA levels increased. Conclusions. By acting probably as a posttranscriptional regulator with a different efficacy on COL2A1 and COL1A2 expression, miR-29b can contribute to the collagens imbalance associated with an abnormal chondrocyte phenotype.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据