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miR‐146a in PBMCs modulates Th1 function in patients with acute coronary syndrome
Author(s) -
Guo Min,
Mao Xiaobo,
Ji Qingwei,
Lang Mingjian,
Li Songnan,
Peng Yudong,
Zhou Wei,
Xiong Bo,
Zeng Qiutang
Publication year - 2010
Publication title -
immunology and cell biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0818-9641
DOI - 10.1038/icb.2010.16
Subject(s) - downregulation and upregulation , peripheral blood mononuclear cell , microrna , acute coronary syndrome , transcription factor , tumor necrosis factor alpha , medicine , immunology , in vitro , cancer research , biology , myocardial infarction , gene , biochemistry
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‐α, MCP‐1, NF‐κB 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.