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Retracted : Downregulated microRNA‐224 aggravates vulnerable atherosclerotic plaques and vascular remodeling in acute coronary syndrome through activation of the TGF‐β/Smad pathway
Author(s) -
Xu HaiMing,
Sui FengHua,
Sun MeiHua,
Guo GongLiang
Publication year - 2019
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.26945
Subject(s) - smad , medicine , transforming growth factor , downregulation and upregulation , endocrinology , microrna , acute coronary syndrome , myocardial infarction , cancer research , biology , biochemistry , gene
Abstract Recent studies have shown that circulating microRNAs (miRNA) play a critical role in diagnosing acute coronary syndrome (ACS). This study aims to investigate the effect of miR‐224 on atherosclerotic plaques forming and vascular remodeling in ACS and its relationship with TGF‐β/Smad pathway. Myocardial infarction (MI) rat model was established and lentivirus vector of miR‐224 inhibitor was prepared for investigating the effect of downregulated miR‐224 on the contents of nitric oxide (NO) and endothelin‐1 (ET‐1), blood lipid levels and inflammatory factor levels in serum as well as the TGF‐β/Smad pathway. The rats suffering from MI had decreased survival rates and exhibited reduced levels of NO, high‐density lipoprotein cholesterol, and lumen diameter, and Smad7 messenger RNA (mRNA) and protein expression; while had significantly increased ratio of heart weight or body weight, levels of ET‐1, inflammatory factors, blood lipid indexes, vascular remodeling indexes, collagen volume fraction, vulnerable atherosclerotic plaque area, VCAM‐1 and MMP‐2 protein expression, TGF‐β, Smad2, Smad3, and Smad4 mRNA and protein expression. After inhibiting the TGF‐β/Smad pathway, the rats suffering from MI showed notably opposite trend. In conclusion, downregulation of miR‐224 expression promotes the formation of vulnerable atherosclerotic plaques and vascular remodeling in ACS through activation of the TGF‐β/Smad pathway. Therefore, this study provides a new therapeutic target for ACS.