Nanog inhibits lipopolysaccharide-induced expression of pro-inflammatory             cytokines by blocking NF-κB transcriptional activity in rat primary microglial             cells.
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.
Neurology Department, The First Affiliated Hospital of Fujian Medical University, Fuzhou, PR China.
Haitao
H
Zhou
Shiyan
S
Chen
Wei
W
Wang
Zhiqiang
Z
Wang
Xiuli
X
Wu
Zhijian
Z
Zhang
D000276:Adjuvants, Immunologic / Q000494:pharmacology; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D002478:Cells, Cultured; D016207:Cytokines / Q000235:genetics / Q000378:metabolism*; D015971:Gene Expression Regulation, Enzymologic / Q000187:drug effects*; D053583:Interleukin-1beta / Q000235:genetics / Q000378:metabolism; D015850:Interleukin-6 / Q000235:genetics / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology; D017628:Microglia / Q000166:cytology / Q000187:drug effects* / Q000201:enzymology*; D016328:NF-kappa B / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D000071317:Nanog Homeobox Protein; D051381:Rats; D011994:Recombinant Proteins / Q000235:genetics / Q000378:metabolism / Q000494:pharmacology; D014157:Transcription Factors / Q000235:genetics / Q000378:metabolism / Q000494:pharmacology*; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism
D000276:Adjuvants, Immunologic; D000893:Anti-Inflammatory Agents; D016207:Cytokines; D053583:Interleukin-1beta; D015850:Interleukin-6; D008070:Lipopolysaccharides; D016328:NF-kappa B; D000071317:Nanog Homeobox Protein; C547030:Nanog protein, rat; D011994:Recombinant Proteins; D014157:Transcription Factors; D014409:Tumor Necrosis Factor-alpha