Experimental cell researchMay 14, 2024

RND3 helps control immune cell response and reduce brain inflammation in Parkinson's disease by blocking NLRP3 inflammasome activation

Gut-Brain Axis Weekly Brief ↗PubMed ↗DOI ↗

Updated Apr 4, 2026

Abstract

RND3 was highly expressed in both the MPTP-induced Parkinson's disease mouse model and BV-2 cells treated with inflammatory stimuli.

RND3 may induce neuroprotective phenotypes in microglia.
Overexpression of RND3 could modulate microglial activation and reduce neuroinflammation.
In vivo experiments indicated that RND3 overexpression alleviated neuroinflammation by inhibiting the NLRP3 inflammasome in the substantia nigra pars compacta.
In vitro results suggested that RND3 reduced pro-inflammatory factor production in BV-2 cells stimulated by inflammatory agents.
Mechanistically, RND3 is associated with decreased activation of the NLRP3 inflammasome in response to inflammation.

Simplified

Neuroinflammation mediated by microglia plays an important role in the etiology of Parkinson's disease (PD). Rho family GTPase 3 (RND3) exerts anti-inflammatory effects and may act as a potential new inducer of neuroprotective phenotypes in microglia. However, whether RND3 can be used to regulate microglia activation or reduce neuroinflammation in PD remains elusive. The study investigated the microglia modulating effects and potential anti-inflammatory effects of RND3 in vivo and in vitro, using animal models of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD and cell models of BV-2 cells stimulated by LPS plus IFN-γ with or without RND3-overexpression. The results showed that RND3 was highly expressed in the MPTP-induced PD mouse model and BV-2 cells treated with LPS and IFN-γ. In vivo experiments confirmed that RND3 overexpression could modulate microglia phenotype and ameliorate MPTP-induced neuroinflammation through inhibiting activation of the NLRP3 inflammasome in substantia nigra pars compacta (SNpc). In vitro study showed that RND3 overexpression could attenuate the production of pro-inflammatory factors in BV2 cells stimulated by LPS and IFN-γ. Mechanistically, RND3 reduced the activation of the NLRP3 inflammasome upon LPS and IFN-γ stimulation. Taken together, these findings suggest that RND3 modulates microglial polarization and alleviates neuroinflammation in Parkinson's disease by suppressing NLRP3 inflammasome activation.

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Declaration of competing interest The authors declare no conflict of interest.

PubMed

RND3 helps control immune cell response and reduce brain inflammation in Parkinson's disease by blocking NLRP3 inflammasome activation

Abstract

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Abstract

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