Differential Expression of Adipokines in Mechanically Stretched‐ Endothelial cells

Abstract

IntroductionHypertension is considered as the major risk factor for cardiovascular diseases, which are the leading cause of morbidity and mortality worldwide. This disease can develop mainly due to the mechanical forces exerted by the blood on the vessels wall. The endothelium, lining the blood vessel, responds to these hemodynamic mechanical forces such as mechanical stretch leading to endothelial dysfunction. Leptin and adiponectin (APN) are two adipokines that are known to be associated with the pathogenesis of hypertension. However, how the level of these hormones is elevated in response to mechanical stretch in endothelial cells is yet to be elucidated.AimIn the present study, we investigated the expression of leptin and adiponectin in endothelial cells exposed to mechanical stretch.MethodsImmortalized human umbilical vein endothelial cells (EA. hy926) were subjected to mechanical stretch (15%, 60 cycle/min and 1Hz) using STREX cell stretching system (STREX Inc., California, USA) for 6, 16 and 24 h. Cultured cells not subjected to stretch (static condition) where used as controls. The mRNA expression of leptin and its receptor (OB‐Rb) as well as APN and adiponectin receptor 2 (APN‐R2) were assessed at different time points using real‐time PCR.ResultsMechanical stretch induced changes in cell morphology in which the cells were elongated and aligned perpendicular to the stretch axis. Stretching of endothelial cells significantly upregulated the expression of leptin after 16 h (0.9515 ± 0.4238‐fold, n=6, p<0.05) and after 24 h (1.577 ± 0.4503‐fold, n=6, p<0.05) of stretching but without affecting the expression of its receptor (OB‐Rb). The mRNA expression of APN also increased significantly in response to 6 h stretching (0.5457 ± 0.1890‐fold, n=6, p<0.05), 16 h stretching (0.9487 ± 0.4058‐fold, n=6, p<0.05) and 24 h stretching (2.664 ± 0.3447, n=6, p<0.0001) compared to unstretched cells, however no change in the expression of APN‐R2 was observed.ConclusionOur findings suggesting that the exposure of endothelial cells to mechanical stretch can result in changes in the expression of adipokines, leptin and adiponectin, will result in better understanding of how vascular biology is affected by mechanical forces and how these molecules can modulate endothelial function in cardiovascular diseases.