Document Detail


Nanog inhibits lipopolysaccharide-induced expression of pro-inflammatory cytokines by blocking NF-κB transcriptional activity in rat primary microglial cells.
MedLine Citation:
PMID:  22200792     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Nanog is an essential transcription factor maintaining the self-renewal and pluripotency of embryonic stem cells, which binds to nuclear factor-κB (NF-κB) proteins, inhibits their transcriptional activity and represses their pro-differentiation activity. The persistent and excessive activation of microglial cells, as primary immune cells in the central nervous system is associated with various nerve system diseases, such as neuropathic pain, ischemia, infection, as well as neurodegenerative diseases. However, the effects of Nanog on the activation of microglial cells have yet to be elucidated. In this study, we investigated whether Nanog inhibits the production of pro-inflammatory factors in lipopolysaccharide (LPS)-stimulated microglial cells. Nanog was shown to down-regulate the mRNA and protein levels of IL-1β, TNF-α and IL-6 in LPS-stimulated rat primary microglial cells. Furthermore, we also found that the transcriptional activity of NF-κB was dramatically reduced by Nanog, which was measured using luciferase assay. The results suggest that Nanog reduces the production of pro-inflammatory cytokines and attenuates inflammatory responses in LPS-stimulated microglial cells by blocking the transcriptional activity of NF-κB. Thus, Nanog may be a potentially useful anti-inflammatory therapy for the treatment of various nervous system diseases.
Authors:
Haitao Zhou; Shiyan Chen; Wei Wang; Zhiqiang Wang; Xiuli Wu; Zhijian Zhang
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2011-12-19
Journal Detail:
Title:  Molecular medicine reports     Volume:  5     ISSN:  1791-3004     ISO Abbreviation:  Mol Med Rep     Publication Date:  2012 Mar 
Date Detail:
Created Date:  2012-01-05     Completed Date:  2012-05-03     Revised Date:  2013-02-22    
Medline Journal Info:
Nlm Unique ID:  101475259     Medline TA:  Mol Med Rep     Country:  Greece    
Other Details:
Languages:  eng     Pagination:  842-6     Citation Subset:  IM    
Affiliation:
Neurology Department, The First Affiliated Hospital of Fujian Medical University, Fuzhou, PR China.
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MeSH Terms
Descriptor/Qualifier:
Adjuvants, Immunologic / pharmacology
Animals
Anti-Inflammatory Agents / pharmacology
Cells, Cultured
Cytokines / genetics,  metabolism*
Gene Expression Regulation, Enzymologic / drug effects*
Interleukin-1beta / genetics,  metabolism
Interleukin-6 / genetics,  metabolism
Lipopolysaccharides / pharmacology
Microglia / cytology,  drug effects*,  enzymology*
NF-kappa B / antagonists & inhibitors,  genetics,  metabolism*
Rats
Recombinant Proteins / genetics,  metabolism,  pharmacology
Transcription Factors / genetics,  metabolism,  pharmacology*
Tumor Necrosis Factor-alpha / genetics,  metabolism
Chemical
Reg. No./Substance:
0/Adjuvants, Immunologic; 0/Anti-Inflammatory Agents; 0/Cytokines; 0/Interleukin-1beta; 0/Interleukin-6; 0/Lipopolysaccharides; 0/NF-kappa B; 0/Nanog protein, rat; 0/Recombinant Proteins; 0/Transcription Factors; 0/Tumor Necrosis Factor-alpha

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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