دورية أكاديمية
أعرض في EDS

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

التفاصيل البيبلوغرافية
العنوان: Inhibition of 26S protease regulatory subunit 7 (MSS1) suppresses neuroinflammation.
المؤلفون: Wei Bi, Xiuna Jing, Lihong Zhu, Yanran Liang, Jun Liu, Lianhong Yang, Songhua Xiao, Anding Xu, Qiaoyun Shi, Enxiang Tao
المصدر: PLoS ONE, Vol 7, Iss 5, p e36142 (2012)
بيانات النشر: Public Library of Science (PLoS), 2012.
سنة النشر: 2012
المجموعة: LCC:Medicine
LCC:Science
مصطلحات موضوعية: Medicine, Science
الوصف: 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.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 1932-6203
Relation: https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22629310/?tool=EBI; https://doaj.org/toc/1932-6203
DOI: 10.1371/journal.pone.0036142
URL الوصول: https://doaj.org/article/1328df7c98714c25be7ce9b5d37006f4
رقم الأكسشن: edsdoj.1328df7c98714c25be7ce9b5d37006f4
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:19326203
DOI:10.1371/journal.pone.0036142