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• W3012129826 abstract "Microglial inflammation is identified as a key process associated with Parkinson's disease (PD) pathogenesis. Our previous study showed that miR-29c-3p (miR-29c) exhibited anti-inflammatory properties in PD animal and neuronal models. However, the specific role and regulatory mechanism of miR-29c played in microglia are still unclear. In this study, lipopolysaccharide (LPS)-stimulated BV-2 cells were used to establish a cellular model of microglial activation for investigating PD. The results showed a decreased expression of miR-29c in LPS-induced BV-2 cells. Over-expression of miR-29c suppressed LPS-triggered Iba-1 increment, pro-inflammatory cytokine release, and NF-кB and TXNIP/NLRP3 inflammasome activation. Silence of miR-29c induced similar effects with LPS on microglial inflammation. In addition, we found that NFAT5 was negatively correlated with miR-29c. Knockdown of NFAT5 blocked the aggravated inflammation in microglia treated by miR-29c inhibitor. Thus, these findings suggest that miR-29c modulates NLRP3 inflammasome to impair microglial inflammatory responses by targeting NFAT5, which represents a promising therapeutic target for PD." @default.
• W3012129826 created "2020-03-23" @default.
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• W3012129826 date "2020-03-30" @default.
• W3012129826 modified "2023-10-16" @default.
• W3012129826 title "miR‐29c‐3p inhibits microglial NLRP3 inflammasome activation by targeting NFAT5 in Parkinson's disease" @default.
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• W3012129826 doi "https://doi.org/10.1111/gtc.12764" @default.
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