Association of adenylate cyclase-associated protein 1 with coronary artery disease
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BackgroundAdenylate cyclase-associated protein 1 (CAP1) is a recently identified receptor for human resistin. As resistin has been related to CAD development and progression and CAP1 has never been evaluated in CAD, the aim of this study was to determine its peripheral blood mononuclear cells (PBMCs) mRNA in patients with CAD, and resistin plasma concentration, PBMCs resistin and CD36 mRNA, considering resistis ability to stimulate CD36 expression invitro. Materials and methodsThis case-controlled study included 27 healthy subjects (CG) and 66 patients requiring coronary angiography. Of the latter, 42 had nonsignificant CAD whereas 24 had significant CAD. Circulating resistin was measured by ELISA; PBMCs CAP1, resistin and CD36 mRNA were determined by real-time PCR. ResultsPatients with significant as well as patients with nonsignificant CAD had significantly higher resistin concentrations compared to the CG (P lt 0 lt bold> lt /bold>001; P=0 lt bold> lt /bold>003). Resistin mRNA did n...ot show significant difference between the investigated groups. CAP1 and CD36 mRNA were significantly higher in significant CAD (P lt 0 lt bold> lt /bold>001; P lt 0 lt bold> lt /bold>001, respectively) and nonsignificant CAD (P lt 0 lt bold> lt /bold>001; P lt 0 lt bold> lt /bold>001, respectively) compared to the CG; significant CAD showed significantly higher CD36 mRNA (P=0 lt bold> lt /bold>040) compared to the nonsignificant CAD group. Multiple linear regression analysis identified Tg and CD36 mRNA as independent predictors of CAP1 (R-2=0 lt bold> lt /bold>402; adjR(2)=0 lt bold> lt /bold>376). ConclusionSignificant up-regulation of PBMCs CAP1, CD36 mRNA and plasma resistin found in significant CAD, as well as in nonsignificant CAD compared to CG, indicates that resistin could be able to exert its effects stronger on cells with up-regulated CAP1 mRNA thus contributing atherosclerosis development.
Keywords:CAP1 / CD36 / coronary artery disease / resistin
Source:European Journal of Clinical Investigation, 2017, 47, 9, 659-666
- Wiley, Hoboken