Suppression of p38/HBP1 pathway alleviates hyperosmotic stress-induced senescent progression of chondrocyte senescence.
- 1 Department of Orthopedic Surgery, The People’s Hospital of China Three Gorges University/The First People’s Hospital of Yichang, Yichang, China.
- # Contributed equally
This study aims to explore the effect of p38 mitogen-activated protein kinase and its downstream target HMG-box transcription factor 1 (HBP1) in the chondrocyte (CH) senescence caused by hyperosmotic stress. Human cartilage tissue with or without osteoarthritis (OA) were collected to detect the differential expression of p38 and HBP1 by Western blot. CHs were isolated from cartilage without OA and used the hyperosmotic medium to accelerate CH senescence in vitro. A p38 inhibitor and siRNA were used to mediate the expression of p38 and HBP1. The viability of CHs was determined by cell counting kit 8 (CCK8) assay. CH-related mRNA expression was analyzed by quantitative real-time polymerase chain reaction (RT-PCR). Immunofluorescence was also used to detect collagen II and beta-galactosidase expression. Senescent cells were increased in both OA cartilage and hyperosmotic stress treatment with a marked upregulation of p38 and HBP1. Suppression of p38 activation reversed the hyperosmotic stress-induced CH senescence and led to an inhibition of HBP1, p16, Runx-2, MMP-13, collagen X expression, and an upregulation of collagen II and SOX-9 expression. Moreover, the silencing of HBP1 also played a protective effect on CH senescence. The suppression of the p38/HBP1 pathway alleviates the hyperosmotic stress-induced senescent progression of CHs.
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HBP1; chondrocyte; osmolality stress; p38; senescence
- Journal Article