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http://dx.doi.org/10.4014/jmb.1507.07103

Alteration of the Metabolome Profile in Endothelial Cells by Overexpression of miR-143/145  

Wang, Wenshuo (Department of Cardiac Surgery, Zhongshan Hospital of Fudan University and Shanghai Institute of Cardiovascular Diseases)
Yang, Ye (Department of Cardiac Surgery, Zhongshan Hospital of Fudan University and Shanghai Institute of Cardiovascular Diseases)
Wang, Yiqing (Department of Cardiothoracic Surgery, Huashan Hospital of Fudan University)
Pang, Liewen (Department of Cardiothoracic Surgery, Huashan Hospital of Fudan University)
Huang, Jiechun (Department of Cardiothoracic Surgery, Huashan Hospital of Fudan University)
Tao, Hongyue (Department of Radiology, Huashan Hospital of Fudan University)
Sun, Xiaotian (Department of Cardiothoracic Surgery, Huashan Hospital of Fudan University)
Liu, Chen (Department of Cardiac Surgery, Zhongshan Hospital of Fudan University and Shanghai Institute of Cardiovascular Diseases)
Publication Information
Journal of Microbiology and Biotechnology / v.26, no.3, 2016 , pp. 572-578 More about this Journal
Abstract
Communication between endothelial cells (ECs) and smooth muscle cells (SMCs) via miR-143/145 clusters is vital to vascular stability. Previous research demonstrates that miR-143/145 released from ECs can regulate SMC proliferation and migration. In addition, a recent study has found that SMCs also have the capability of manipulating EC function via miR-143/145. In the present study, we artificially increased the expression of miR-143/145 in ECs, to mimic a similar change caused by miR-143/145 released by SMCs, and applied untargeted metabolomics analysis, aimed at investigating the consequential effect of miR-143/145 overexpression. Our results showed that miR-143/145 overexpression alters the levels of metabolites involved in energy production, DNA methylation, and oxidative stress. These changed metabolites indicate that metabolic pathways, such as the SAM cycle and TCA cycle, exhibit significant differences from the norm with miR-143/145 overexpression.
Keywords
Smooth muscle cell; untargeted metabolomics; cellular communication; vascular biology; microRNA;
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