Circulating resistin protein and mRNA concentrations and clinical severity of coronary artery disease

Abstract

IntroductionPrevious studies have implicated a strong link between circulating plasma resistin and coronary artery disease (CAD). The aim of this study was to evaluate the differences in peripheral blood mononuclear cells (PBMC) resistin mRNA and its plasma protein concentrations between the patients with CAD of different clinical severity.Material and methodsThis study included 33 healthy subjects as the control group (CG) and 77 patients requiring coronary angiography. Of the latter 30 was CAD negative whereas 47 were CAD positive [18 with stable angina pectoris (SAP) and 29 with acute coronary syndrome (ACS)]. Circulating resistin was measured by ELISA; PBMC resistin mRNA was determined by real-time PCR.ResultsResistin protein was significantly higher in the ACS group compared to the CG (P = 0.001) and the CAD negative group (P = 0.018). Resistin mRNA expression did not vary across the study groups, despite the positive correlation seen with plasma resistin (ρ = 0.305, P = 0.008). In patients, plasma resistin and PBMC resistin mRNA negatively correlated with HDL-C (ρ = -0.404, P < 0.001 and ρ = -0.257, P = 0.032, respectively). Furthermore, the highest plasma resistin tertile showed the lowest HDL-C (P = 0.006). Plasma resistin was positively associated with serum creatinine (ρ = 0.353, P = 0.002).ConclusionSignificant increase of plasma resistin in patients with ACS compared to CG and CAD negative patients was observed. Despite no change in PBMC resistin mRNA in different disease conditions a positive association between resistin mRNA and resistin plasma protein was evident. Both plasma resistin and PBMC resistin mRNA were negatively associated with plasma HDL-C, and plasma resistin positively with serum creatinine.

SGK1 is modulated by resistin in vascular smooth muscle cells and in the aorta following diet‐induced obesity

“…High plasma resistin concentration is implicated in clinical and experimental models of cardiovascular diseases. A positive correlation between plasma resistin and the severity of coronary artery disease was observed in a recent clinical study (19). Further, overexpression of resistin was observed to increase atherosclerotic lesion progression in the ldlr knockout mice (20).…”

Association of adenylate cyclase‐associated protein 1 with coronary artery disease

“…Namely, it has been shown that resistin is secreted from macrophages, in atheroma, locally and abundantly where it exerts its effects within atherosclerotic lesions in a paracrine manner, so during plaque destabilisation, resistin protein could be additionally released from the plaque itself [2,10]. Namely, it has been shown that resistin is secreted from macrophages, in atheroma, locally and abundantly where it exerts its effects within atherosclerotic lesions in a paracrine manner, so during plaque destabilisation, resistin protein could be additionally released from the plaque itself [2,10].…”

“…The CG was comprised of 27 healthy subjects (12 males and 15 females), who were selected among 67 healthy volunteers, after thorough assessment of their health status, and review of their medical history to determine the presence or absence of cardiovascular disease, as described elsewhere [10].…”

“…Twelve-hour fasting whole blood was drawn from all subjects, and serum and plasma were isolated, analysed and stored as described elsewhere [10]. Resistin protein concentrations, creatinine, glucose, lipid parameters [total cholesterol (TC), HDL-C, LDL-C, triglycerides (Tg)], high-sensitivity C-reactive protein (hsCRP), fasting insulin concentrations and homoeostasis model assessment of insulin resistance (HOMA-IR) were assayed as described elsewhere [10].…”

“…Twelve-hour fasting whole blood was drawn from all subjects, and serum and plasma were isolated, analysed and stored as described elsewhere [10]. Resistin protein concentrations, creatinine, glucose, lipid parameters [total cholesterol (TC), HDL-C, LDL-C, triglycerides (Tg)], high-sensitivity C-reactive protein (hsCRP), fasting insulin concentrations and homoeostasis model assessment of insulin resistance (HOMA-IR) were assayed as described elsewhere [10]. PBMCs collection from plasma samples, and downstream total RNA isolation and RNA quality and quantity assessment was performed as described elsewhere (only samples with 260/280 absorbance ratio > 1Á8 and 260/230 absorbance ratio > 2Á0, with clearly visible 18S and 28S ribosomal RNA bands were used in downstream experiments), [10].…”