title: miR-146a in PBMCs modulates Th1 function in patients with acute coronary syndrome.
abstract: The upregulation of Th1 cells has been suggested to have an essential function in the development of atherosclerosis (AS). Recent studies indicate that miR-146a is a microRNA specifically and highly expressed in Th1-driven autoimmune disease. The aim of the study was to investigate the possible mechanisms of the miR-146a in the onset of acute coronary syndrome (ACS). The results showed that the expression of miR-146a in peripheral blood mononuclear cells (PBMCs) was significantly increased in patients with ACS. We showed that overexpression of miR-146a in PBMCs could significantly upregulate the function of Th1 cells. Furthermore, we showed that miR-146a treatment could modulate the Th1 differentiation through posttranscriptional enhancing the T-bet pathway in PBMCs. In addition, this study also provided evidence that miR-146a treatment in vitro could induce the protein expression of TNF-alpha, MCP-1, NF-kappaB p65, which are key pro-inflammatory cytokines and critical transcription factor in AS. In contrast, miR-146a inhibitor could attenuate these phenomena significantly. The results support the concept that miR-146a may be a novel regulatory factor in Th1 differentiation and a new therapeutic target for AS and ACS.
authors.affiliation: Department of Cardiology, Institute of Cardiovascular Disease, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
authors.forename: Min
authors.initials: M
authors.lastname: Guo
authors.forename: Xiaobo
authors.initials: X
authors.lastname: Mao
authors.forename: Qingwei
authors.initials: Q
authors.lastname: Ji
authors.forename: Mingjian
authors.initials: M
authors.lastname: Lang
authors.forename: Songnan
authors.initials: S
authors.lastname: Li
authors.forename: Yudong
authors.initials: Y
authors.lastname: Peng
authors.forename: Wei
authors.initials: W
authors.lastname: Zhou
authors.forename: Bo
authors.initials: B
authors.lastname: Xiong
authors.forename: Qiutang
authors.initials: Q
authors.lastname: Zeng
mesh_terms: D054058:Acute Coronary Syndrome / Q000209:etiology / Q000235:genetics / Q000276:immunology*; D050197:Atherosclerosis / Q000150:complications / Q000235:genetics / Q000276:immunology*; D015153:Blotting, Western; D002454:Cell Differentiation / Q000276:immunology; D002469:Cell Separation; D016207:Cytokines / Q000096:biosynthesis; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D007249:Inflammation / Q000235:genetics / Q000276:immunology; D007963:Leukocytes, Mononuclear / Q000276:immunology*; D008297:Male; D035683:MicroRNAs / Q000276:immunology*; D008875:Middle Aged; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015398:Signal Transduction / Q000276:immunology; D018417:Th1 Cells / Q000166:cytology / Q000276:immunology*
chemical_list: D016207:Cytokines; C542542:MIRN146 microRNA, human; D035683:MicroRNAs