Effects of thyroxine on adhesion molecules and proinflammatory cytokines secretion on human umbilical vein endothelial cells

lt;p gt;Thyroid dysfunction is associated with elevated cardiovascular risk factors and atherosclerosis. It could be suggested that, hyperthyroidism is related to a higher prevalence of arterial abnormalities. Therefore, evaluating the endothelial dysfunction (ED) related biomarkers seem to be an important issue. It is not clear whether endothelial cells are biologically responsive to thyroid hormones (THs) or how THs induces the production of endothelial cells (EC)derived proinflammatory mediators. Hence, in this study the effects of thyroxine (T lt;sub gt;4 lt;/sub gt;) on ED and inflammatory related mediators were evaluated. Human umbilical vein endothelial cells was used as endothelial cell model which was treated with concentrations of 50, 100, 200 nmol/L of T lt;sub gt;4 lt;/sub gt; in various exposure times. In the following, gene and protein expression levels of ECrelated markers including intercellular adhesion molecule1 (ICAM1), vascular endothelial growth factor (VEGF), and Eselectin were determined using real time polymerase chain reaction (RTPCR) and western blotting methods. Also, interleukin6 (IL6) and tumor necrosis factor (TNFα) protein levels as proinflammatory cytokines were determined by enzyme linked immunosorbent assay (ELISA) method.  Gene and protein expression analysis revealed that T lt;sub gt;4 lt;/sub gt; treatments up regulated the levels of VEGF, ICAM1, and Eselectin as ED markers. In addition, T lt;sub gt;4 lt;/sub gt;treated cells had higher significant levels of IL6 and TNFα versus untreated cells in different incubation times. This study proposed the atherosclerotic effects of thyroid hormone. Based on our findings, T lt;sub gt;4 lt;/sub gt; had strong effects on the gene and protein expression levels of proinflammatory, angiogenesis, and ED major mediators associated with atherosclerosis development. lt;/p gt;