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- Xue Wang, Heyu Meng, Jianjun Ruan, Weiwei Chen, and Fanbo Meng.
- Jilin Provincial Precision Medicine Key Laboratory for Cardiovascular Genetic Diagnosis (Jilin Provincial Engineering Laboratory for Endothelial Function and Genetic Diagnosis of Cardiovascular Disease, Jilin Provincial Molecular Biology Research Center for Precision Medicine of Major Cardiovascular Disease, Jilin Provincial Cardiovascular Research Institute), Department of Cardiology, The Third Hospital of Jilin University, Changchun, China.
- Medicine (Baltimore). 2021 Jan 22; 100 (3): e23468.
BackgroundThe G0/G1 switch 2 (G0S2) gene is closely related to lipolysis, cell proliferation, apoptosis, oxidative phosphorylation, and the development of a variety of tumors. The aim of the present study was to expand the sample size to confirm the relationship between the expression of the G0S2 gene in peripheral blood and acute myocardial infarction (AMI) based on previous gene chip results.MethodsThree hundred patients were initially selected, of which 133 were excluded in accordance with the exclusion criteria. Peripheral blood leukocytes were collected from 92 patients with AMI and 75 patients with stable coronary atherosclerotic disease (CAD). mRNA expression levels of G0S2 in peripheral blood leukocytes was measured by RT-PCR, and protein expression levels by Western blot analysis. The results of these assays in the 2 groups were compared.ResultsmRNA expression levels of GOS2 in the peripheral blood leukocytes of patients with AMI were 0.41-fold lower than those of patients with stable CAD (P < .05), and GOS2 protein expression levels were 0.45-fold lower. Multivariate logistic regression analysis indicated that low expression levels of the G0S2 gene increased the risk of AMI by 2.08-fold in stable CAD patients.ConclusionsG0S2 gene expression in the peripheral blood leukocytes of AMI patients was lower than that of stable CAD patients. Low G0S2 gene expression in peripheral blood leukocytes is an independent risk factor for AMI in stable CAD patients.Copyright © 2021 the Author(s). Published by Wolters Kluwer Health, Inc.
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