Expression of renin-angiotensin system on dendritic cells of patients with coronary artery disease.

Dendritic cells (DCs) and renin-angiotensin system (RAS) have both been reported to contribute to the pathogenesis of atherosclerosis. Recently researches find the RAS expression on DCs and its effect on DCs' differentiation and proinflammatory function. The pattern of RAS expression on DCs derived from normal monocytes vs that on DCs derived from cornoary artery diease was investigated. In 82 coronary artery disease (CAD) patients and healthy controls (CTL), expressions of angiotensin I-converting enzyme (ACE), angiotensin AT1 receptor and DC-specific ICAM-3-grabbing nonintegrin (DC-SIGN) on DCs were measured by western-blot: CAD patients had an increased expression of ACE, AT1 receptor and DC-SIGN compared to controls especially in acute myocardial infarction (AMI). Cardiovascular risk factors of cardiovascular disease and circulating anigotensin II (Ang II) were assessed and found increased in AMI compared with CTL. The DC-SIGN and high-sensitivity C-reactive protein (hsCRP) also had significant correlations with RAS expression on DCs. Our research demonstrated the RAS expressions on DCs and their increase in CAD especially AMI. The RAS activation on DCs may cause a series of changes such as enhancing recruitment of DCs, activating the T cells and increasing their proinflammtory functions. The recruitment and T cells contact ability of DCs increases through DC-SIGN may be one of pathogenesis of atherosclerosis and this function may promoted by tissue RAS. CRP may also have some effect to the local RAS exprssion on DCs.