Research Paper Volume 11, Issue 16 pp 6371—6384
MiR-27a promotes the autophagy and apoptosis of IL-1β treated-articular chondrocytes in osteoarthritis through PI3K/AKT/mTOR signaling
- 1 Department of Spine Surgery, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong, China
- 2 Department of Spine Surgery, The Third Affliated Hospital of Southern Medical University, Guangzhou, Guangdong, China
- 3 Department of Cell Biology, School of Basic Medical Science, Southern Medical University, Guangzhou, Guangdong, China
Received: June 27, 2019 Accepted: August 10, 2019 Published: August 27, 2019https://doi.org/10.18632/aging.102194
How to Cite
Copyright © 2019 Cai et al. This is an open-access article distributed under the terms of the Creative Commons Attribution (CC BY 3.0) License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Osteoarthritis (OA) is a common degenerative joint disorder, which involves articular cartilage degeneration as well as joint inflammatory reactions. The recent studies have identified microRNA (miRNA) as one of the epigenetic mechanisms for the regulation of gene expression. Here we aim to reveal the role of miRNA in the regulation of gene expression in articular chondrocytes and its significance in the OA pathogenesis. In the present study, miRNA profiling was performed using OA cartilage and normal healthy cartilage tissues. As compared to their levels in normal cells and tissues, miR-27a expression was found to be upregulated in OA cartilage and IL-1β-treated articular chondrocytes. TUNEL staining, as well as flow cytometry with Annexin V-FITC/PI double labeling indicated that miR-27a inhibition reduced the apoptosis of IL-1β-treated articular chondrocytes. Bioinformatics prediction and the dual-luciferase reporter assay indicated that miR-27a targeted the 3′-UTR of the PI3K gene to silence it. The PI3K mRNA level in OA cartilage and IL-1β-treated articular chondrocytes was also downregulated, comparing with normal cells and tissues. Transfection of chondrocytes transfected with the miR-27a inhibitor upregulated the PI3K expression. This study demonstrated miR-27a is a regulator of the PI3K-Akt-mTOR axis in human chondrocytes and could participate in OA pathogenesis.