Open AccessEffects of autophagy on apoptosis of articular chondrocytes in adjuvant arthritis rats
Author(s) -
Zhou Renpeng,
Zhu Fei,
Wu Xiaoshan,
Song Sujing,
Chen Yong,
Zhu Chuanjun,
Dai Beibei,
Qian Xuewen,
Wang Ke,
Hu Wei,
Chen Feihu
Publication year - 2019
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.14629
Subject(s) - autophagy , chondrocyte , apoptosis , in vivo , arthritis , in vitro , rheumatoid arthritis , cancer research , chemistry , cartilage , programmed cell death , microbiology and biotechnology , medicine , immunology , biology , anatomy , biochemistry
Rheumatoid arthritis (RA) is a chronic, systemic autoimmune disease that eventually leads to joint deformities and loss of joint function. Previous studies have demonstrated a close relationship between autophagy and the development of RA. Although autophagy and apoptosis are two different forms of programmed death, the relationship between them in relation to RA remains unclear. In this study, we explored the effect of autophagy on apoptosis of articular chondrocytes in vivo and in vitro. Adjuvant arthritis (AA) and acid‐induced primary articular chondrocyte apoptosis were used as in vivo and in vitro models, respectively. Articular chondrocyte autophagy and apoptosis were both observed dynamically in AA rat articular cartilage at different stages (15 days, 25 days and 35 days). Moreover, chondrocyte apoptosis and articular cartilage injury in AA rats were increased by the autophagy inhibitor 3‐methyladenine (3‐MA) and decreased by the autophagy activator rapamycin. In addition, pre‐treatment with 3‐MA increased acid‐induced chondrocyte apoptosis, while pre‐treatment with rapamycin reduced acid‐induced chondrocyte apoptosis in vitro. These results suggest that autophagy might be a potential target for the treatment of RA.