Dehydroepiandrosterone inhibits ADAMTS expression via an ERK-dependent mechanism in chondrocytes.

Autor: Huang K; Department of Orthopedic Surgery, Tongde Hospital of Zhejiang Province, Hangzhou, China., Cheng L; Department of Orthopedic Surgery, Tongde Hospital of Zhejiang Province, Hangzhou, China., Jiang C; Department of Orthopedic Surgery, Tongde Hospital of Zhejiang Province, Hangzhou, China., Zheng C; Department of Orthopedic Surgery, Tongde Hospital of Zhejiang Province, Hangzhou, China., Cai H; Department of Ultrasound, The 903rd Hospital of PLA, Hangzhou, China.
Jazyk: angličtina
Zdroj: PloS one [PLoS One] 2024 Nov 22; Vol. 19 (11), pp. e0313560. Date of Electronic Publication: 2024 Nov 22 (Print Publication: 2024).
DOI: 10.1371/journal.pone.0313560
Abstrakt: Osteoarthritis (OA) is a joint disease in which cartilage degradation is the hallmark pathological change. In this study, we investigated the anti-osteoarthritic effects of DHEA in rabbit chondrocytes. Polymerase chain reaction was performed to evaluate the expression of a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS)-4, ADAMTS-5, aggrecan and collagen type 2. In addition, ERK1/2 signaling pathway components were analyzed by Western blotting. In IL-1β-induced chondrocytes, the phosphorylation of ERK1/2 was enhanced, and the downstream catabolic genes, including ADAMTS-4 and ADAMTS-5, were upregulated, while the anabolic genes aggrecan and collagen type 2 were downregulated. DHEA administration restored the IL-1β-induced imbalance in anabolic and catabolic gene expression. In addition, the phosphorylation of ERK1/2 was suppressed by DHEA. Then, PD98059 was used to block the ERK1/2 signaling pathway. The protective effect of DHEA was significantly increased when ERK1/2 signaling was inactivated. DHEA may exert its protective effect by suppressing ADAMTS in an ERK1/2-dependent manner in rabbit chondrocytes.
Competing Interests: The authors have declared that no competing interests exist.
(Copyright: © 2024 Huang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)
Databáze: MEDLINE
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