Heyu Meng1, Xue Wang1, Jianjun Ruan1, Weiwei Chen1, Fanbo Meng1, Ping Yang1. 1. 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, China-Japan Union Hospital of Jilin University, Changchun, China.
Abstract
Aims: The present study was designed to evaluate whether the expression of the suppressor of cytokine signaling 3 (SOCS3) gene could serve as a biomarker to predict the risk of acute myocardial infarction (AMI). Basic Methods: Peripheral white blood cells were collected from 113 patients with AMI and 92 patients with stable coronary artery disease (SCAD). SOCS3 mRNA expression levels in peripheral blood cells were determined by a real-time quantitative polymerase chain reaction, and levels of the SOCS3 protein were determined by Western blotting. Results: The mRNA expression levels of the SOCS3 gene in AMI patients was 1.33-fold higher than that in the SCAD patients, and the level of the SOCS3 protein was 1.25-fold higher (p < 0.05 for both). Bivariate logistic regression analysis documented that elevated expression of the SOCS3 gene was an independent risk factor for AMI. A regression analysis demonstrated a lack of correlation between elevated expression levels of SOCS3 and the levels of fasting blood glucose high- and low-density lipoprotein, and cardiac troponin. Conclusions: Elevated expression of the SOCS3 gene results most likely from enhanced inflammatory responses and is an independent risk factor for AMI.
Aims: The present study was designed to evaluate whether the expression of the suppressor of cytokine signaling 3 (SOCS3) gene could serve as a biomarker to predict the risk of acute myocardial infarction (AMI). Basic Methods: Peripheral white blood cells were collected from 113 patients with AMI and 92 patients with stable coronary artery disease (SCAD). SOCS3 mRNA expression levels in peripheral blood cells were determined by a real-time quantitative polymerase chain reaction, and levels of the SOCS3 protein were determined by Western blotting. Results: The mRNA expression levels of the SOCS3 gene in AMI patients was 1.33-fold higher than that in the SCAD patients, and the level of the SOCS3 protein was 1.25-fold higher (p < 0.05 for both). Bivariate logistic regression analysis documented that elevated expression of the SOCS3 gene was an independent risk factor for AMI. A regression analysis demonstrated a lack of correlation between elevated expression levels of SOCS3 and the levels of fasting blood glucose high- and low-density lipoprotein, and cardiac troponin. Conclusions: Elevated expression of the SOCS3 gene results most likely from enhanced inflammatory responses and is an independent risk factor for AMI.