The p66shc gene expression in peripheral blood monocytes is increased in patients with coronary artery disease

Abstract

Background: The p66shc protein has been shown to control cellular responses to oxidative stress, being involved in atherosclerosis in animal models. However, the relationship between the p66shc gene expression levels and coronary artery disease (CAD) in humans remains unknown. In this study,we examined whether the p66shc 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 p66shc 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 p66shc 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 p66shc gene expression levels in PBMs were significantly higher in CAD patients compared with non-CAD subjects. Multiple stepwise regression analysis revealed that the p66shc gene expression levels and hypertension medication were independently related to CAD (R2 = 0.287). Further, the p66shc gene expression 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 p66shc gene expression in PBMs is independently associated with CAD in Japanese subjects. The p66shc gene expression level in PBMs may be a novel biomarker of CAD in humans. © 2010 Wiley Periodicals, Inc.