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Caveolin-1 knockout improves CFA-induced inflammatory pain in adult mice through modulating the cGAS STING pathway
Huan Chang1, Cancan Cheng1, Ning Zheng1
1Department of Anesthesiology, The Third Xiangya Hospital, Central South University, Changsha, China.
Background:
Inflammatory pain poses a significant clinical challenge, with its underlying mechanisms not yet fully elucidated. This study investigated the role of Caveolin-1 (Cav1) in inflammatory pain and elucidated its molecular mechanisms.
Methods:
We analyzed public databases and employed a mouse model of inflammatory pain induced by complete Freund's adjuvant (CFA). Cav1-knockout (Cav1-/-) mice were used to evaluate Cav1's function. The study incorporated behavioral tests, immunohistochemistry and molecular analyses. BV2 microglial cells served as the in vitro model.
Results:
Following CFA injection, Cav1 expression was markedly elevated in the dorsal horn of spinal cord, correlating with pain behavior and inflammatory responses. Cav1-/- mice demonstrated significantly reduced pain behavior and inflammatory responses after CFA induction. Mechanistically, Cav1 enhanced inflammation by activating the cGAS-STING pathway and inhibiting autophagy. In BV2 microglia, Cav1 overexpression increased proinflammatory cytokine expression (TNF-α, IL-1β, IL-6) while inhibiting autophagy, whereas Cav1 knockdown produced opposing effects.
Conclusion:
This study reveals a novel role of Cav1 in inflammatory pain, demonstrating its regulation of inflammation through modulation of the cGAS-STING pathway and autophagy. These findings advance our understanding of the pathogenesis of inflammatory pain and identify Cav1 as a potential therapeutic target.
Insights
Caveolin-1 (Cav1) exacerbates inflammatory pain by activating the cGAS-STING pathway and inhibiting autophagy. Targeting Cav1 may offer a new therapeutic strategy for managing inflammatory pain.
Area of Science:
- Neuroscience
- Immunology
- Molecular Biology
Background:
- Inflammatory pain is a complex condition with incompletely understood mechanisms.
- Caveolin-1 (Cav1) is investigated for its role in inflammatory pain pathogenesis.
Purpose of the Study:
- To elucidate the role and molecular mechanisms of Cav1 in inflammatory pain.
- To determine Cav1's impact on inflammatory responses and pain behavior.
Main Methods:
- Utilized a mouse model of inflammatory pain induced by complete Freund's adjuvant (CFA).
- Employed Cav1-knockout mice and BV2 microglial cells for in vitro and in vivo analyses.
- Conducted behavioral tests, immunohistochemistry, and molecular analyses.
Main Results:
- Cav1 expression increased in the spinal cord dorsal horn post-CFA injection, correlating with pain.
- Cav1 knockout mice showed reduced pain behavior and inflammation.
- Cav1 activated the cGAS-STING pathway and inhibited autophagy, increasing pro-inflammatory cytokines.
Conclusions:
- Cav1 plays a significant role in inflammatory pain by modulating the cGAS-STING pathway and autophagy.
- Cav1 inhibition presents a potential therapeutic target for inflammatory pain.
- Findings enhance understanding of inflammatory pain mechanisms.
