title: miR-22 contributes to the pathogenesis of patients with coronary artery disease by targeting MCP-1: An observational study.
abstract: The aim of this study is to determine miR-22 expression levels in peripheral blood mononuclear cells (PBMCs) of patients with coronary artery disease (CAD) and to investigate whether MCP-1 expression is regulated by miR-22. miR-22 expression in PBMCs from 60 CAD patients including stable angina pectoris (SAP) (n = 29), unstable angina pectoris (UAP) or non-ST elevation myocardial infarction (NSTEMI) (n = 17), or ST-elevation MI (STEMI) (n = 14) and 20 non-CAD subjects by real-time polymerase chain reaction (qRT-PCR). The luciferase activity assays were employed to determine whether miR-22 binds to 3'UTR of MCP-1. miR-22 mimics and inhibitors were transfected into healthy PBMCs. MCP-1 mRNA and protein levels were determined by qRT-PCR and enzyme-linked immuno sorbent assay, respectively. The qRT-PCR results showed that miR-22 levels in PBMCs were decreased in CAD patients, and MCP-1 was augmented in CAD patients and was inversely correlated with miR-22 levels. The luciferase activity assays indicated that MCP-1 was a target of miR-22. Overexpression of miR-22 could significantly repress MCP-1 expression at both mRNA and protein levels in PBMCs, whereas inhibition of miR-22 showed the opposite effects. This study revealed that miR-22 is downregulated in PBMCs from patients with CAD and that miR-22 may participate in inflammatory response by targeting MCP-1, therefore contributing CAD.
authors.affiliation: Department of Cardiology, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, Guangdong, China.
authors.forename: Bairong
authors.initials: B
authors.lastname: Chen
authors.forename: Liyun
authors.initials: L
authors.lastname: Luo
authors.forename: Weiping
authors.initials: W
authors.lastname: Zhu
authors.forename: Xiaoliang
authors.initials: X
authors.lastname: Wei
authors.forename: Songbiao
authors.initials: S
authors.lastname: Li
authors.forename: Yin
authors.initials: Y
authors.lastname: Huang
authors.forename: Mao
authors.initials: M
authors.lastname: Liu
authors.forename: Xiufang
authors.initials: X
authors.lastname: Lin
mesh_terms: D000368:Aged; D016022:Case-Control Studies; D018932:Chemokine CCL2 / Q000502:physiology*; D003324:Coronary Artery Disease / Q000209:etiology*; D005260:Female; D006801:Humans; D007963:Leukocytes, Mononuclear / Q000378:metabolism; D008297:Male; D035683:MicroRNAs / Q000502:physiology*; D008875:Middle Aged; D060888:Real-Time Polymerase Chain Reaction; D015854:Up-Regulation
chemical_list: C111835:CCL2 protein, human; D018932:Chemokine CCL2; C548375:MIRN22 microRNA, human; D035683:MicroRNAs