Loss of SCRG1 in chondrocytes inhibits osteoarthritis by promoting autophagy activity in the temporomandibular joint through inhibition of neurokine receptors

Abstract

Background: To investigate in vitro how scrapie responsive gene 1 (SCRG1) contributes to the development of temporomandibular joint osteoarthritis (TMJOA).

Methods: Western blotting was used to identify protein expression. Proinflammatory cytokine levels were assessed by means of an enzyme-linked immunosorbent test. In order to find out whether chondrocytes expressed protein light chain 3B (LC3B), immunofluorescence was utilized.

Results: In the TMJOA in vitro model, hydrogen peroxide (H₂O₂) treatment increased the expression of SCRG1, stimulated chondrocyte catabolism and inflammatory response, and blocked autophagy. In chondrocytes, SCRG1 silencing reduces the inflammatory response, catabolism, and autophagy inhibition brought on by H₂O₂. Concurrently, H₂O₂ induction triggers the nuclear factor (NF)-κB pathway and nerve growth factor receptor (NGFR). When SCRG1 is downregulated, NGFR expression is inhibited and the NF-κB pathway is blocked.

Conclusions: By inhibiting NGFR and blocking the NF-κB pathway, knocking down SCRG1 can prevent H₂O₂-induced inflammatory response, metabolic breakdown and autophagy inhibition in chondrocytes.

Keywords: Autophagy; Catabolism; Inflammation; NF-κB; NGFR; SCRG1; TMJOA.