title: The miR-30a Negatively Regulates IL-17-Mediated Signal Transduction by Targeting Traf3ip2.
abstract: Interleukin-17 (IL-17) has been proved to be involved in the pathogenesis of several autoimmune diseases, including lupus, rheumatoid arthritis, multiple sclerosis, and inflammatory bowel disease. The regulation of IL-17 signal transduction is less studied. miR-30a has been identified to be downregulated in these human autoimmune diseases and their related animal models. However, how it functions in IL-17-mediated inflammation and the pathogenesis of these diseases remain unknown. In this study, we showed that miR-30a inhibits IL-17-mediated NF-κB and MAPK activation, leading to the reduced production of inflammatory cytokines and chemokines. miR-30a also reduced mRNA stability triggered by IL-17 stimulation. These suppressive effects of miR-30a were mediated by directly targeting Traf3ip2 mRNA (coding for Act1). Thus, we concluded that the downregulation of miR-30a in autoimmune diseases may exacerbate IL-17-mediated inflammation, which may serve as a potential target for the therapy of these diseases.
authors.affiliation: 1 State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital of Medical College, Zhejiang University , Hangzhou, Zhejiang Province, People's Republic of China .
authors.forename: Qun
authors.initials: Q
authors.lastname: Wan
authors.affiliation: 3 The National Education Base for Basic Medical Sciences, School of Medicine, Zhejiang University , Hangzhou, Zhejiang Province, People's Republic of China .
authors.forename: Zhuo
authors.initials: Z
authors.lastname: Zhou
authors.affiliation: 1 State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital of Medical College, Zhejiang University , Hangzhou, Zhejiang Province, People's Republic of China .|2 Collaborative Innovation Center for Diagnosis and Treatment of Infectious Disease , Hangzhou, Zhejiang Province, People's Republic of China .|3 The National Education Base for Basic Medical Sciences, School of Medicine, Zhejiang University , Hangzhou, Zhejiang Province, People's Republic of China .
authors.forename: Shiping
authors.initials: S
authors.lastname: Ding
authors.affiliation: 1 State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital of Medical College, Zhejiang University , Hangzhou, Zhejiang Province, People's Republic of China .|2 Collaborative Innovation Center for Diagnosis and Treatment of Infectious Disease , Hangzhou, Zhejiang Province, People's Republic of China .
authors.forename: Jianqin
authors.initials: J
authors.lastname: He
mesh_terms: D048868:Adaptor Proteins, Signal Transducing; D001327:Autoimmune Diseases / Q000235:genetics* / Q000276:immunology; D045744:Cell Line, Tumor; D016207:Cytokines / Q000096:biosynthesis; D015536:Down-Regulation; D004789:Enzyme Activation / Q000276:immunology; D006367:HeLa Cells; D006801:Humans; D007249:Inflammation / Q000276:immunology; D020381:Interleukin-17 / Q000276:immunology*; D020935:MAP Kinase Signaling System / Q000276:immunology*; D035683:MicroRNAs / Q000235:genetics*; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism; D016328:NF-kappa B / Q000276:immunology; D012333:RNA, Messenger / Q000235:genetics; D047988:Tumor Necrosis Factor Receptor-Associated Peptides and Proteins / Q000096:biosynthesis* / Q000235:genetics
chemical_list: D048868:Adaptor Proteins, Signal Transducing; D016207:Cytokines; D020381:Interleukin-17; C546086:MIRN30b microRNA, human; D035683:MicroRNAs; D016328:NF-kappa B; D012333:RNA, Messenger; C414202:TRAF3IP2 protein, human; D047988:Tumor Necrosis Factor Receptor-Associated Peptides and Proteins; D020928:Mitogen-Activated Protein Kinases