Inhibition of Long Non-Coding RNA KCNQ1OT1 Attenuates Neuroinflammation and Neuronal Apoptosis Through Regulating NLRP3 Expression via Sponging miR-30e-3p
Aixia Song,1 Yuying Yang,2 Hongmei He,1 Jian Sun,1 Qing Chang,1 Qian Xue1 1Department of Neurology, The First Affiliated Hospital of Hebei North University, Zhangjiakou, Hebei, 075000, People’s Republic of China; 2Stroke Office, The First Affiliated Hospital of Hebei North University, Zhan...
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Dove Medical Press
2021
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oai:doaj.org-article:036830bd8e2f4c8492e8d0000a3810fc2021-12-02T14:47:43ZInhibition of Long Non-Coding RNA KCNQ1OT1 Attenuates Neuroinflammation and Neuronal Apoptosis Through Regulating NLRP3 Expression via Sponging miR-30e-3p1178-7031https://doaj.org/article/036830bd8e2f4c8492e8d0000a3810fc2021-05-01T00:00:00Zhttps://www.dovepress.com/inhibition-of-long-non-coding-rna-kcnq1ot1-attenuates-neuroinflammatio-peer-reviewed-fulltext-article-JIRhttps://doaj.org/toc/1178-7031Aixia Song,1 Yuying Yang,2 Hongmei He,1 Jian Sun,1 Qing Chang,1 Qian Xue1 1Department of Neurology, The First Affiliated Hospital of Hebei North University, Zhangjiakou, Hebei, 075000, People’s Republic of China; 2Stroke Office, The First Affiliated Hospital of Hebei North University, Zhangjiakou, Hebei, 075000, People’s Republic of ChinaCorrespondence: Qian XueDepartment of Neurology, The First Affiliated Hospital of Hebei North University, No. 12 Changqing Road, Qiaoxi District, Zhangjiakou, Hebei, 075000, People’s Republic of ChinaEmail qianyanxin7@163.comBackground: Neuroinflammation and neuronal apoptosis are considered as the critical factors in the pathogenesis of multiple neurological diseases. Recent studies have shown that long non-coding RNA (lncRNA) plays a crucial part in neuroinflammation and neuronal apoptosis.Methods: The expression levels of lncRNA KCNQ1OT1, miR-30e-3p and NLRP3 in lipopolysaccharide (LPS)-induced HMC3 cells were analyzed using RT-qPCR. MTT assay, LDH release assay and ELISA were used to assess the effect of KCNQ1OT1 and miR-30e-3p on neuroinflammation and neuronal apoptosis. The targeted regulatory relationships among KCNQ1OT1, miR-30e-3p and NLRP3 were evaluated by bioinformatics analysis, dual-luciferase reporter gene assay, RT-qPCR and Western blot.Results: In LPS-induced HMC3 cells, the expression levels of KCNQ1OT1 and NLRP3 were increased, while the expression level of miR-30e-3p was reduced. Knockdown of KCNQ1OT1 alleviated LPS-induced apoptosis and neuroinflammation of HMC3 cells, accompanied by increased cell viability, low LDH release and reduced cell apoptosis rate, and reduced levels of TNF-α, IL-1β and IL-6. Overexpression of miR-30e-3p had a similar effect. Additionally, KCNQ1OT1 could bind with miR-30e-3p and repress its expression in HMC3 cells, and KCNQ1OT1 overexpression counteracted miR-30e-3p’s inhibitory effect on LPS-induced neuronal damage and inflammatory response in HMC3 cells. Furthermore, KCNQ1OT1 could positively regulate the expression of NLRP3 via repressing miR-30e-3p.Conclusion: Inhibition of KCNQ1OT1 could reduce neuroinflammation and neuronal apoptosis induced by LPS in HMC3 cells by regulating miR-30e-3p/NLRP3 pathway, suggesting that KCNQ1OT1 and miR-30e-3p could serve as promising therapeutic targets for treating neurological diseases.Keywords: NLRP3, KCNQ1OT1, miR-30e-3p, neuroinflammationSong AYang YHe HSun JChang QXue QDove Medical Pressarticlenlrp3kcnq1ot1mir-30e-3p;neuroinflammationPathologyRB1-214Therapeutics. PharmacologyRM1-950ENJournal of Inflammation Research, Vol Volume 14, Pp 1731-1742 (2021) |
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nlrp3 kcnq1ot1 mir-30e-3p;neuroinflammation Pathology RB1-214 Therapeutics. Pharmacology RM1-950 |
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nlrp3 kcnq1ot1 mir-30e-3p;neuroinflammation Pathology RB1-214 Therapeutics. Pharmacology RM1-950 Song A Yang Y He H Sun J Chang Q Xue Q Inhibition of Long Non-Coding RNA KCNQ1OT1 Attenuates Neuroinflammation and Neuronal Apoptosis Through Regulating NLRP3 Expression via Sponging miR-30e-3p |
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Aixia Song,1 Yuying Yang,2 Hongmei He,1 Jian Sun,1 Qing Chang,1 Qian Xue1 1Department of Neurology, The First Affiliated Hospital of Hebei North University, Zhangjiakou, Hebei, 075000, People’s Republic of China; 2Stroke Office, The First Affiliated Hospital of Hebei North University, Zhangjiakou, Hebei, 075000, People’s Republic of ChinaCorrespondence: Qian XueDepartment of Neurology, The First Affiliated Hospital of Hebei North University, No. 12 Changqing Road, Qiaoxi District, Zhangjiakou, Hebei, 075000, People’s Republic of ChinaEmail qianyanxin7@163.comBackground: Neuroinflammation and neuronal apoptosis are considered as the critical factors in the pathogenesis of multiple neurological diseases. Recent studies have shown that long non-coding RNA (lncRNA) plays a crucial part in neuroinflammation and neuronal apoptosis.Methods: The expression levels of lncRNA KCNQ1OT1, miR-30e-3p and NLRP3 in lipopolysaccharide (LPS)-induced HMC3 cells were analyzed using RT-qPCR. MTT assay, LDH release assay and ELISA were used to assess the effect of KCNQ1OT1 and miR-30e-3p on neuroinflammation and neuronal apoptosis. The targeted regulatory relationships among KCNQ1OT1, miR-30e-3p and NLRP3 were evaluated by bioinformatics analysis, dual-luciferase reporter gene assay, RT-qPCR and Western blot.Results: In LPS-induced HMC3 cells, the expression levels of KCNQ1OT1 and NLRP3 were increased, while the expression level of miR-30e-3p was reduced. Knockdown of KCNQ1OT1 alleviated LPS-induced apoptosis and neuroinflammation of HMC3 cells, accompanied by increased cell viability, low LDH release and reduced cell apoptosis rate, and reduced levels of TNF-α, IL-1β and IL-6. Overexpression of miR-30e-3p had a similar effect. Additionally, KCNQ1OT1 could bind with miR-30e-3p and repress its expression in HMC3 cells, and KCNQ1OT1 overexpression counteracted miR-30e-3p’s inhibitory effect on LPS-induced neuronal damage and inflammatory response in HMC3 cells. Furthermore, KCNQ1OT1 could positively regulate the expression of NLRP3 via repressing miR-30e-3p.Conclusion: Inhibition of KCNQ1OT1 could reduce neuroinflammation and neuronal apoptosis induced by LPS in HMC3 cells by regulating miR-30e-3p/NLRP3 pathway, suggesting that KCNQ1OT1 and miR-30e-3p could serve as promising therapeutic targets for treating neurological diseases.Keywords: NLRP3, KCNQ1OT1, miR-30e-3p, neuroinflammation |
format |
article |
author |
Song A Yang Y He H Sun J Chang Q Xue Q |
author_facet |
Song A Yang Y He H Sun J Chang Q Xue Q |
author_sort |
Song A |
title |
Inhibition of Long Non-Coding RNA KCNQ1OT1 Attenuates Neuroinflammation and Neuronal Apoptosis Through Regulating NLRP3 Expression via Sponging miR-30e-3p |
title_short |
Inhibition of Long Non-Coding RNA KCNQ1OT1 Attenuates Neuroinflammation and Neuronal Apoptosis Through Regulating NLRP3 Expression via Sponging miR-30e-3p |
title_full |
Inhibition of Long Non-Coding RNA KCNQ1OT1 Attenuates Neuroinflammation and Neuronal Apoptosis Through Regulating NLRP3 Expression via Sponging miR-30e-3p |
title_fullStr |
Inhibition of Long Non-Coding RNA KCNQ1OT1 Attenuates Neuroinflammation and Neuronal Apoptosis Through Regulating NLRP3 Expression via Sponging miR-30e-3p |
title_full_unstemmed |
Inhibition of Long Non-Coding RNA KCNQ1OT1 Attenuates Neuroinflammation and Neuronal Apoptosis Through Regulating NLRP3 Expression via Sponging miR-30e-3p |
title_sort |
inhibition of long non-coding rna kcnq1ot1 attenuates neuroinflammation and neuronal apoptosis through regulating nlrp3 expression via sponging mir-30e-3p |
publisher |
Dove Medical Press |
publishDate |
2021 |
url |
https://doaj.org/article/036830bd8e2f4c8492e8d0000a3810fc |
work_keys_str_mv |
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