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Association of adenylate cyclase‐associated protein 1 with coronary artery disease
Author(s) -
Munjas Jelena,
Sopić Miron,
SpasojevićKalimanovska Vesna,
KalimanovskaOštrić Dimitra,
Anđelković Kristina,
JelićIvanović Zorana
Publication year - 2017
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/eci.12787
Subject(s) - resistin , peripheral blood mononuclear cell , medicine , coronary artery disease , endocrinology , messenger rna , biology , in vitro , adipokine , gene , insulin resistance , biochemistry , insulin
Background Adenylate cyclase‐associated protein 1 ( CAP 1) is a recently identified receptor for human resistin. As resistin has been related to CAD development and progression and CAP 1 has never been evaluated in CAD , the aim of this study was to determine its peripheral blood mononuclear cells ( PBMC s) mRNA in patients with CAD , and resistin plasma concentration, PBMC s resistin and CD 36 mRNA , considering resistiǹs ability to stimulate CD 36 expression in vitro . Materials and methods This 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 ; PBMC s CAP 1, resistin and CD 36 mRNA were determined by real‐time PCR . Results Patients with significant as well as patients with nonsignificant CAD had significantly higher resistin concentrations compared to the CG ( P < 0·001; P = 0·003). Resistin mRNA did not show significant difference between the investigated groups. CAP 1 and CD 36 mRNA were significantly higher in significant CAD ( P < 0·001; P < 0·001, respectively) and nonsignificant CAD ( P < 0·001; P < 0·001, respectively) compared to the CG ; significant CAD showed significantly higher CD 36 mRNA ( P = 0·040) compared to the nonsignificant CAD group. Multiple linear regression analysis identified Tg and CD 36 mRNA as independent predictors of CAP 1 ( R 2 = 0·402; adj R 2 = 0·376). Conclusion Significant up‐regulation of PBMC s CAP 1, CD 36 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 CAP 1 mRNA thus contributing atherosclerosis development.