Open AccessThe p66 shc Gene Expression in Peripheral Blood Monocytes Is Increased in Patients With Coronary Artery Disease
Author(s) -
Noda Yoshihiro,
Yamagishi Shoichi,
Matsui Takanori,
Ueda So,
Ueda Shinichiro,
Jinnouchi Yuko,
Hirai Yuji,
Imaizumi Tsutomu
Publication year - 2010
Publication title -
clinical cardiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.263
H-Index - 72
eISSN - 1932-8737
pISSN - 0160-9289
DOI - 10.1002/clc.20761
Subject(s) - medicine , coronary artery disease , gene expression , percutaneous coronary intervention , cardiology , coronary angiography , cad , gastroenterology , gene , myocardial infarction , biochemistry , chemistry , engineering drawing , engineering
Background The p66 shc protein has been shown to control cellular responses to oxidative stress, being involved in atherosclerosis in animal models. However, the relationship between the p66 shc gene expression levels and coronary artery disease (CAD) in humans remains unknown. In this study, we examined whether the p66 shc gene expression in peripheral blood monocytes (PBMs) was increased in patients with CAD, compared with age‐ and sex‐matched subjects without CAD. Hypothesis We hypothesize that the p66 shc gene expression level in PBMs is increased in patients with CAD. Methods Forty consecutive Japanese subjects who underwent coronary angiography for suspected CAD were enrolled in this study. The p66 shc gene expression levels in PBMs were quantitatively measured by real‐time reverse transcription‐polymerase chain reactions. Uni‐ and multivariate analyses were applied for the correlates of CAD. CAD was diagnosed if there was > 75% obstruction of at least 1 major coronary artery or a history of percutaneous coronary intervention. Results There were no significant differences of blood chemistries and clinical characteristics between the patients with and without CAD, except the number of subjects who were on hypertension medication. The p66 shc gene expression levels in PBMs were significantly higher in CAD patients compared with non‐CAD subjects. Multiple stepwise regression analysis revealed that the p66 shc gene expression levels and hypertension medication were independently related to CAD (R 2 =0.287). Further, the p66 shc gene expres‐ sion levels were significantly increased ( P < 0.05) in proportion to the number of diseased vessels. Conclusions The present study is the first demonstration that increased the p66 shc gene expression in PBMs is independently associated with CAD in Japanese subjects. The p66 shc gene expression level in PBMs may be a novel biomarker of CAD in humans. Copyright © 2010 Wiley Periodicals, Inc. This work was supported in part by Grants of Collaboration with Venture Companies Project from the Ministry of Education, Culture, Sports, Science and Technology, Japan (S. Yamagishi). The authors have no other funding, financial relationships, or conflicts of interest to disclose.