Bax Targeted by miR-29a Regulates Chondrocyte Apoptosis in Osteoarthritis

Author:

Miao Guiqiang12,Zang Xuehui2,Hou Huige1,Sun Hui2,Wang Lihui2,Zhang Ting2,Tan Yongtao2,Liu Wenzhou2,Ye Pei2,Gao Lihua2ORCID,Zha Zhengang1ORCID

Affiliation:

1. Department of Orthopedics, The First Affiliated Hospital of Jinan University, Guangzhou 510630, China

2. Department of Orthopedics, Nanhai Hospital of Southern Medical University and Foshan Nanhai District People’s Hospital, Guangdong 528200, China

Abstract

Osteoarthritis (OA) is a chronic degenerative joint disease, where chondrocyte apoptosis is responsible for cartilage degeneration. Bax is a well-known proapoptotic protein of the Bcl-2 family, involved in a large number of physiological and pathological processes. However, the regulation mechanisms of Bax underlying chondrocyte apoptosis in OA remain unknown. In the present study, we determined the role of Bax in human OA and chondrocyte apoptosis. The results showed that Bax was upregulated in chondrocytes from the articular cartilage of OA patients and in cultured chondrocyte-like ATDC5 cells treated by IL-1β. Bax was identified to be the direct target of miR-29a by luciferase reporter assay and by western blotting. Inhibition of miR-29a by the mimics protested and overexpression by miR-29a inhibitors aggravated ATDC5 apoptosis induced by IL-1β. These data reveal that miR-29a/Bax axis plays an important role in regulating chondrocyte apoptosis and suggest that targeting the proapoptotic protein Bax and increasing expression levels of miR-29a emerge as potential approach for protection against the development of OA.

Publisher

Hindawi Limited

Subject

General Immunology and Microbiology,General Biochemistry, Genetics and Molecular Biology,General Medicine

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