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miR-29c-3p inhibits microglial NLRP3 inflammasome activation by targeting NFAT5 in Parkinson's disease.
Genes to Cells ( IF 1.3 ) Pub Date : 2020-03-11 , DOI: 10.1111/gtc.12764 Ruili Wang 1 , Qing Li 1 , Ya He 1 , Ying Yang 1 , Qiaoya Ma 1 , Chen Li 1
Genes to Cells ( IF 1.3 ) Pub Date : 2020-03-11 , DOI: 10.1111/gtc.12764 Ruili Wang 1 , Qing Li 1 , Ya He 1 , Ying Yang 1 , Qiaoya Ma 1 , Chen Li 1
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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.
中文翻译：
miR-29c-3p通过靶向帕金森氏病中的NFAT5来抑制小胶质NLRP3炎性小体活化。
小胶质细胞炎症被认为是与帕金森氏病（PD）发病机理相关的关键过程。我们以前的研究表明，miR-29c-3p（miR-29c）在PD动物和神经元模型中表现出抗炎特性。然而，miR- 29c在小胶质细胞中发挥的具体作用和调控机制仍不清楚。在这项研究中，脂多糖（LPS）刺激的BV-2细胞被用于建立小胶质细胞激活的细胞模型以研究PD。结果显示，LPS诱导的BV-2细胞中miR‐29c的表达降低。miR-29c的过表达抑制LPS触发的Iba-1增量，促炎性细胞因子释放以及NF-кB和TXNIP / NLRP3炎性体激活。miR-29c沉默可导致LPS对小胶质细胞炎症产生相似的作用。此外，我们发现NFAT5与miR-29c呈负相关。敲除NFAT5可以阻断miR-29c抑制剂治疗的小胶质细胞的炎症加重。因此，这些发现表明，miR- 29c通过靶向NFAT5来调节NLRP3炎性小体，从而损害小胶质细胞的炎症反应，这代表了PD的有希望的治疗靶标。
更新日期：2020-03-11
中文翻译：
miR-29c-3p通过靶向帕金森氏病中的NFAT5来抑制小胶质NLRP3炎性小体活化。
小胶质细胞炎症被认为是与帕金森氏病（PD）发病机理相关的关键过程。我们以前的研究表明，miR-29c-3p（miR-29c）在PD动物和神经元模型中表现出抗炎特性。然而，miR- 29c在小胶质细胞中发挥的具体作用和调控机制仍不清楚。在这项研究中，脂多糖（LPS）刺激的BV-2细胞被用于建立小胶质细胞激活的细胞模型以研究PD。结果显示，LPS诱导的BV-2细胞中miR‐29c的表达降低。miR-29c的过表达抑制LPS触发的Iba-1增量，促炎性细胞因子释放以及NF-кB和TXNIP / NLRP3炎性体激活。miR-29c沉默可导致LPS对小胶质细胞炎症产生相似的作用。此外，我们发现NFAT5与miR-29c呈负相关。敲除NFAT5可以阻断miR-29c抑制剂治疗的小胶质细胞的炎症加重。因此，这些发现表明，miR- 29c通过靶向NFAT5来调节NLRP3炎性小体，从而损害小胶质细胞的炎症反应，这代表了PD的有希望的治疗靶标。
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