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

TL;DR

This study shows that reducing SCRG1 in chondrocytes can prevent osteoarthritis by blocking inflammation and promoting autophagy in the temporomandibular joint.

Contribution

The novel finding is that SCRG1 inhibition prevents osteoarthritis by suppressing NGFR and the NF-κB pathway in chondrocytes.

Findings

SCRG1 silencing reduces H2O2-induced inflammation and catabolism in chondrocytes.

SCRG1 downregulation promotes autophagy and inhibits the NF-κB pathway.

Blocking SCRG1 expression inhibits NGFR and prevents joint degeneration in TMJOA.

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.

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