miR‐29c‐3p inhibits microglial NLRP3 inflammasome activation by targeting NFAT5 in Parkinson's disease
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‐2...
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| Published in | Genes to cells : devoted to molecular & cellular mechanisms Vol. 25; no. 6; pp. 364 - 374 |
|---|---|
| Main Authors | , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
Wiley Subscription Services, Inc
01.06.2020
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| Subjects | |
| Online Access | Get full text |
| ISSN | 1356-9597 1365-2443 1365-2443 |
| DOI | 10.1111/gtc.12764 |
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| 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.
miR‐29c protects against microglial activation of PD. miR‐29c suppresses NLRP3 inflammasome activation by targeting NFAT5. |
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| AbstractList | 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. 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.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. 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. miR‐29c protects against microglial activation of PD. miR‐29c suppresses NLRP3 inflammasome activation by targeting NFAT5. |
| Author | Li, Chen Wang, Ruili Ma, Qiaoya He, Ya Li, Qing Yang, Ying |
| Author_xml | – sequence: 1 givenname: Ruili surname: Wang fullname: Wang, Ruili organization: The Second Affiliated Hospital of Xi’an Jiaotong University – sequence: 2 givenname: Qing surname: Li fullname: Li, Qing organization: The Second Affiliated Hospital of Xi’an Jiaotong University – sequence: 3 givenname: Ya surname: He fullname: He, Ya organization: The Second Affiliated Hospital of Xi’an Jiaotong University – sequence: 4 givenname: Ying surname: Yang fullname: Yang, Ying organization: The Second Affiliated Hospital of Xi’an Jiaotong University – sequence: 5 givenname: Qiaoya surname: Ma fullname: Ma, Qiaoya organization: The Second Affiliated Hospital of Xi’an Jiaotong University – sequence: 6 givenname: Chen orcidid: 0000-0002-6050-4775 surname: Li fullname: Li, Chen email: cfine818xjtu@126.com organization: The Second Affiliated Hospital of Xi’an Jiaotong University |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/32160394$$D View this record in MEDLINE/PubMed |
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| Keywords | NFAT5 Parkinson's disease NLRP3 inflammasome microglia miR-29c-3p |
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| Snippet | Microglial inflammation is identified as a key process associated with Parkinson's disease (PD) pathogenesis. Our previous study showed that miR‐29c‐3p... Microglial inflammation is identified as a key process associated with Parkinson's disease (PD) pathogenesis. Our previous study showed that miR-29c-3p... |
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| SubjectTerms | Animal models Inflammasomes Inflammation Lipopolysaccharides Microglia miR‐29c‐3p Movement disorders Neurodegenerative diseases NFAT5 NLRP3 inflammasome Parkinson's disease Therapeutic applications |
| Title | miR‐29c‐3p inhibits microglial NLRP3 inflammasome activation by targeting NFAT5 in Parkinson's disease |
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