ArticleEXCLI journal2025
The regulatory role and mechanism of TRPV3 on apoptosis and inflammation in osteoarthritis.
Article in EXCLI journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- The Role of the C-Reactive Protein-Triglyceride Glucose Index in Predicting New-Onset Chronic Diseases: Evidence From a Longitudinal Cohort Study.Brain and behavior · 2026Article
- Ion channels as therapeutic targets in osteoarthritis.Trends in pharmacological sciences · 2025Review
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3 authors.
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Abstract
Osteoarthritis (OA) is one of the most common forms of degenerative joint disease characterized by persistent pain, inflammation of the joints, and restricted range of motion among the elderly worldwide. Interleukin-1 beta (IL-1β) is increased in the injured joints and contributes to the OA pathobiology by inducing chondrocyte apoptosis and inflammation. Transient receptor potential (TRP) ion channels have recently been reported as potential players in the modulation of apoptosis and inflammation. Here, we aimed to understand the regulatory role and effect of TRPV3 on apoptosis and inflammation in osteoarthritis by using C28/I2 chondrocyte cells as a model. Chondrocytes were transfected with TRPV3-specific siRNA for 24 hours and then stimulated with IL-1β in vitro. Cell cycle progression and apoptosis were evaluated with flow cytometry. The levels of TRPV3, apoptotic (Bax, Caspase-3, and Bcl-2), and inflammatory (iNOS, COX-2) genes were measured by quantitative real-time polymerase chain reaction (qRT-PCR) and confirmed with western blot. Treatment of the C28/I2 chondrocyte cells with IL-1β resulted in the over-expression of TRPV3, induction of apoptosis, and over-expression of inflammation indices. Knockdown of TRPV3 significantly reduced the expression of Bax and Caspase 3 proapoptotic factors while increasing the expression of the Bcl-2 antiapoptotic factor in the mRNA and protein levels in the IL-1β-stimulated cells. Its knockdown also decreased the expression of the inflammatory factors iNOS and COX-2 in mRNA and protein levels, confirming that TRPV3 knockdown hinders apoptosis and inflammation in IL-1β-stimulated chondrocytes. In conclusion, we demonstrated that si-TRPV3 treatment significantly mitigates IL-1β-related effects on the C28/I2 chondrocyte cells. These findings suggested that TRPV3 could be an effective target for the treatment of OA. See also the graphical abstract(Fig. 1).
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