Inhibition of 26S protease regulatory subunit 7 (MSS1) suppresses neuroinflammation.

Recently, researchers have focused on immunosuppression induced by rifampicin. Our previous investigation found that rifampicin was neuroprotective by inhibiting the production of pro-inflammatory mediators, thereby suppressing microglial activation. In this study, using 2-dimensional gel electropho...

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Autores principales:	Wei Bi, Xiuna Jing, Lihong Zhu, Yanran Liang, Jun Liu, Lianhong Yang, Songhua Xiao, Anding Xu, Qiaoyun Shi, Enxiang Tao
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2012
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/1328df7c98714c25be7ce9b5d37006f4
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spelling	oai:doaj.org-article:1328df7c98714c25be7ce9b5d37006f42021-11-18T07:18:03ZInhibition of 26S protease regulatory subunit 7 (MSS1) suppresses neuroinflammation.1932-620310.1371/journal.pone.0036142https://doaj.org/article/1328df7c98714c25be7ce9b5d37006f42012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22629310/?tool=EBIhttps://doaj.org/toc/1932-6203Recently, researchers have focused on immunosuppression induced by rifampicin. Our previous investigation found that rifampicin was neuroprotective by inhibiting the production of pro-inflammatory mediators, thereby suppressing microglial activation. In this study, using 2-dimensional gel electrophoresis (2-DE) and mass spectrometry (MS), we discovered that 26S protease regulatory subunit 7 (MSS1) was decreased in rifampicin-treated microglia. Western blot analysis verified the downregulation of MSS1 expression by rifampicin. As it is indicated that the modulation of the ubiquitin-26S proteasome system (UPS) with proteasome inhibitors is efficacious for the treatment of neuro-inflammatory disorders, we next hypothesized that silencing MSS1 gene expression might inhibit microglial inflammation. Using RNA interference (RNAi), we showed significant reduction of IkBα degradation and NF-kB activation. The production of lipopolysaccharides-induced pro-inflammatory mediators such as inducible nitric oxide synthase (iNOS), nitric oxide, cyclooxygenase-2, and prostaglandin E(2) were also reduced by MSS1 gene knockdown. Taken together, our findings suggested that rifampicin inhibited microglial inflammation by suppressing MSS1 protein production. Silencing MSS1 gene expression decreased neuroinflammation. We concluded that MSS1 inhibition, in addition to anti-inflammatory rifampicin, might represent a novel mechanism for the treatment of neuroinflammatory disorders.Wei BiXiuna JingLihong ZhuYanran LiangJun LiuLianhong YangSonghua XiaoAnding XuQiaoyun ShiEnxiang TaoPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 5, p e36142 (2012)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Wei Bi Xiuna Jing Lihong Zhu Yanran Liang Jun Liu Lianhong Yang Songhua Xiao Anding Xu Qiaoyun Shi Enxiang Tao Inhibition of 26S protease regulatory subunit 7 (MSS1) suppresses neuroinflammation.
description	Recently, researchers have focused on immunosuppression induced by rifampicin. Our previous investigation found that rifampicin was neuroprotective by inhibiting the production of pro-inflammatory mediators, thereby suppressing microglial activation. In this study, using 2-dimensional gel electrophoresis (2-DE) and mass spectrometry (MS), we discovered that 26S protease regulatory subunit 7 (MSS1) was decreased in rifampicin-treated microglia. Western blot analysis verified the downregulation of MSS1 expression by rifampicin. As it is indicated that the modulation of the ubiquitin-26S proteasome system (UPS) with proteasome inhibitors is efficacious for the treatment of neuro-inflammatory disorders, we next hypothesized that silencing MSS1 gene expression might inhibit microglial inflammation. Using RNA interference (RNAi), we showed significant reduction of IkBα degradation and NF-kB activation. The production of lipopolysaccharides-induced pro-inflammatory mediators such as inducible nitric oxide synthase (iNOS), nitric oxide, cyclooxygenase-2, and prostaglandin E(2) were also reduced by MSS1 gene knockdown. Taken together, our findings suggested that rifampicin inhibited microglial inflammation by suppressing MSS1 protein production. Silencing MSS1 gene expression decreased neuroinflammation. We concluded that MSS1 inhibition, in addition to anti-inflammatory rifampicin, might represent a novel mechanism for the treatment of neuroinflammatory disorders.
format	article
author	Wei Bi Xiuna Jing Lihong Zhu Yanran Liang Jun Liu Lianhong Yang Songhua Xiao Anding Xu Qiaoyun Shi Enxiang Tao
author_facet	Wei Bi Xiuna Jing Lihong Zhu Yanran Liang Jun Liu Lianhong Yang Songhua Xiao Anding Xu Qiaoyun Shi Enxiang Tao
author_sort	Wei Bi
title	Inhibition of 26S protease regulatory subunit 7 (MSS1) suppresses neuroinflammation.
title_short	Inhibition of 26S protease regulatory subunit 7 (MSS1) suppresses neuroinflammation.
title_full	Inhibition of 26S protease regulatory subunit 7 (MSS1) suppresses neuroinflammation.
title_fullStr	Inhibition of 26S protease regulatory subunit 7 (MSS1) suppresses neuroinflammation.
title_full_unstemmed	Inhibition of 26S protease regulatory subunit 7 (MSS1) suppresses neuroinflammation.
title_sort	inhibition of 26s protease regulatory subunit 7 (mss1) suppresses neuroinflammation.
publisher	Public Library of Science (PLoS)
publishDate	2012
url	https://doaj.org/article/1328df7c98714c25be7ce9b5d37006f4
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Inhibition of 26S protease regulatory subunit 7 (MSS1) suppresses neuroinflammation.

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