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


OBJECTIVE
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.
Noda
Yoshihiro
Y
Department of Internal Medicine, Division of Cardio-Vascular Medicine, Kurume, Japan.
Yamagishi
Sho-ichi
S
Matsui
Takanori
T
Ueda
So
S
Ueda
Shin-ichiro
S
Jinnouchi
Yuko
Y
Hirai
Yuji
Y
Imaizumi
Tsutomu
T
D000368:Aged; D003324:Coronary Artery Disease / Q000097:blood / Q000235:genetics*; D003430:Cross-Sectional Studies; D005260:Female; D015870:Gene Expression / Q000235:genetics*; D006801:Humans; D007564:Japan; D016015:Logistic Models; D008297:Male; D009000:Monocytes / Q000378:metabolism*; D015999:Multivariate Analysis; D012044:Regression Analysis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D055765:Shc Signaling Adaptor Proteins / Q000235:genetics*; D000071425:Src Homology 2 Domain-Containing, Transforming Protein 1; D013223:Statistics as Topic
C528024:SHC1 protein, human; D055765:Shc Signaling Adaptor Proteins; D000071425:Src Homology 2 Domain-Containing, Transforming Protein 1