The expression of p66shc in peripheral blood monocytes is increased in patients with coronary heart disease and correlated with endothelium-dependent vasodilatation

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• 作者：Qin Miao ; Qiong Wang ; Lini Dong ; Yanjiao Wang ; Yi Tan ; Xiangyu Zhang
• 关键词：p66shc ; Endothelium ; dependent vasodilatation ; Coronary heart disease ; Peripheral blood monocytes ; Homocysteine
• 刊名：Heart and Vessels
• 出版年：2015
• 出版时间：July 2015
• 年：2015
• 卷：30
• 期：4
• 页码：451-457
• 全文大小：504 KB
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• 作者单位：Qin Miao (1) (2)
  Qiong Wang (1)
  Lini Dong (1)
  Yanjiao Wang (1)
  Yi Tan (3)
  Xiangyu Zhang (1)
  
  1. Department of Geriatrics, Second Xiangya Hospital of Central South University, No. 139, Middle Renmin Road, Changsha, 410011, Hunan, People’s Republic of China
  2. Department of Geriatrics, Changsha Central hospital, Changsha, 410001, Hunan, People’s Republic of China
  3. Department of Ultrasound, Second Xiangya Hospital of Central South University, Changsha, 410011, Hunan, People’s Republic of China
  
• 刊物类别：Medicine
• 刊物主题：Medicine & Public Health
  Cardiology
  Cardiac Surgery
  Vascular Surgery
  Biomedical Engineering
  Interventional Radiology
  Ultrasound
  
• 出版者：Springer Japan
• ISSN：1615-2573

文摘

The objective of this study is to detect the p66shc mRNA and protein expression of the peripheral blood monocytes (PBMs) in coronary heart disease patients (CHD) and controls, to evaluate the correlation between the expression of p66shc mRNA in the PBMs and endothelium-dependent vasodilatation. This study included 78 coronary angiography-documented CHD patients (CHD group) and 38 non-CHD controls (control group). The p66shc mRNA and protein levels were determined by quantitative real-time PCR and western blotting. The flow-mediated dilatation (FMD, endothelium-dependent), nitroglycerine-induced dilatation (NID, endothelium-independent) and carotid intimal medial thickness (CIMT) were detected using high-resolution ultrasound. The p66shc mRNA and the protein expression levels in the PBMs were significantly higher in the CHD group compared with the control group (p?=?0.007 and 0.001). The FMD (p?<?0.001) and NID (p?=?0.013) were significantly lower and the CIMT (p?=?0.007) was significantly thicker in the CHD patients than in the controls. In the univariate analysis, the expression of the p66shc mRNA in the PBMs was significantly positively correlated with the serum LDL-C and homocysteine levels and the CIMT and was inversely correlated with the FMD and the NID (all p?<?0.001). In the multiple linear regression analysis, the FMD (p?<?0.001), LDL-C (p?=?0.002) and homocysteine levels (p?=?0.002) remained independently correlated with the p66shc mRNA expression. These findings highlight a pivotal role for the expression of p66shc in CHD and endothelial dysfunction, which might represent a molecular target to prevent endothelial dysfunction-related disease.