Effects of autophagy on apoptosis of articular chondrocytes in adjuvant arthritis rats

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...

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Bibliographic Details
Published in:Journal of cellular and molecular medicine 2019-11, Vol.23 (11), p.7879-7884
Main Authors: Zhou, Renpeng, Zhu, Fei, Wu, Xiaoshan, Song, Sujing, Chen, Yong, Zhu, Chuanjun, Dai, Beibei, Qian, Xuewen, Wang, Ke, Hu, Wei, Chen, Feihu
Format: Article
Language:English
Subjects:
3‐methyladenine
Adenine - analogs & derivatives
Adenine - pharmacology
Animals
Apoptosis
Apoptosis - drug effects
Arthritis
Arthritis, Experimental - pathology
Autoimmune diseases
Autophagy
Autophagy - drug effects
Cartilage (articular)
Cartilage, Articular - pathology
Cells, Cultured
chondrocyte
Chondrocytes
Chondrocytes - drug effects
Chondrocytes - pathology
Collagen
Disease Models, Animal
Experiments
Homeostasis
Inflammation
Male
Phagocytosis
Rapamycin
Rats, Sprague-Dawley
Rheumatoid arthritis
Short Communication
Short Communications
Sirolimus - pharmacology
Variance analysis
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Summary: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.
ISSN:1582-1838
1582-4934
DOI:10.1111/jcmm.14629