title: Mouse pyrin and HIN domain family member 1 (pyhin1) protein positively regulates LPS-induced IFN-β and NO production in macrophages.
abstract: The pyrin and HIN-domain (PYHIN) family member1 (pyhin1) is a member of PYHIN proteins and involved in transcriptional regulation of genes important for cell cycle control, differentiation and apoptosis. The regulatory action of mouse pyhin1 on LPS-induced inflammatory response was examined. LPS augmented the pyhin1 mRNA expression in murine RAW 264.7 macrophage cells and peritoneal macrophages. The augmentation of pyhin1 mRNA expression was abolished by parthenolide, a NF-κB inhibitor. Silencing of pyhin1 with small interfering RNA reduced the production of IFN-β and NO. However, pyhin1 silencing did not affect the production of TNF-α, IL-6, IL-10 and prostaglandin E2. Reduced IFN-β production by pyhin1 silencing caused inactivation of STAT1 and reduced expression of IRF1. Pyhin1 silencing inhibited the expression of TRAF6, TBK1 and TRIF, which trigger IFN-β production in the MyD88-independent pathway. However, pyhin1 silencing did not affect the expression of MyD88, IRAK4 and several mitogen-activated protein kinases in the MyD88-dependent pathway. Taken together, mouse pyhin1 was suggested to be a NF-κB-responsible gene in response to LPS and positively regulate LPS-induced IFN-β and NO production through up-regulating the MyD88-independent signaling pathway.
authors.affiliation: Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Aichi, Japan.
authors.forename: Abedul
authors.initials: A
authors.lastname: Haque
authors.forename: Naoki
authors.initials: N
authors.lastname: Koide
authors.forename: Erdenezaya
authors.initials: E
authors.lastname: Odkhuu
authors.forename: Bilegtsaikhan
authors.initials: B
authors.lastname: Tsolmongyn
authors.forename: Yoshikazu
authors.initials: Y
authors.lastname: Naiki
authors.forename: Takayuki
authors.initials: T
authors.lastname: Komatsu
authors.forename: Tomoaki
authors.initials: T
authors.lastname: Yoshida
authors.forename: Takashi
authors.initials: T
authors.lastname: Yokochi
mesh_terms: D000818:Animals; D002460:Cell Line; D005786:Gene Expression Regulation / Q000187:drug effects; D007249:Inflammation / Q000276:immunology; D050856:Interferon Regulatory Factor-1 / Q000235:genetics / Q000378:metabolism; D016899:Interferon-beta / Q000378:metabolism*; D008070:Lipopolysaccharides / Q000276:immunology; D017737:Macrophages, Peritoneal / Q000276:immunology*; D051379:Mice; D016328:NF-kappa B / Q000037:antagonists & inhibitors; D009569:Nitric Oxide / Q000378:metabolism*; D009687:Nuclear Proteins / Q000235:genetics / Q000378:metabolism*; D034741:RNA, Small Interfering / Q000235:genetics; D050794:STAT1 Transcription Factor / Q000235:genetics / Q000378:metabolism; D012717:Sesquiterpenes / Q000494:pharmacology; D015398:Signal Transduction / Q000187:drug effects; D048029:TNF Receptor-Associated Factor 6 / Q000235:genetics / Q000378:metabolism
chemical_list: D050856:Interferon Regulatory Factor-1; D016899:Interferon-beta; D008070:Lipopolysaccharides; D016328:NF-kappa B; D009569:Nitric Oxide; D009687:Nuclear Proteins; D034741:RNA, Small Interfering; D050794:STAT1 Transcription Factor; D012717:Sesquiterpenes; D048029:TNF Receptor-Associated Factor 6; C494258:Irf1 protein, mouse; C000592086:Ifi209 protein, Mouse; C002669:parthenolide
keywords: MyD88-independent pathway; Pyhin1; interferon-β; lipopolysaccharide; nitric oxide