Effects Of Thyroid Stimulating Hormone (TSH) On Function And Mechanism Of Human Umbilical Vein Endothelial Cells

Objective:Hypothyroidism is well known to be associated with atherosclerosis. The underlying mechanism is widely thought to be TH deficiency. However, atherosclerosis has also been observed in patients with subclinical hypothyroidism(SCH), in which TSH is elevated but TH stays with in its normal range. Thus, the development of atherosclerosis in SCH cannot be explained only by the role of TH. Endothelial dysfunction has been implicated the first step in the development of atherosclerosis. In the present study, we designed to examine that TSH, by binding to TSHR on human umbilical vein endothelial cells, plays an important role in atherosclerosis.Methods:Real-time qPCR were used to measure the mRNA expression of genes after treatment with different concentrations of TSH. For stimulation experiments, HUVECs were cultured in serum free medium and stimulated with TSH for the indicated time and concentrations.Results:Compared to the normal group, a time and dose-dependent decress in the levels of eNOS and PGI2 mRNA expression were observed(P<0.05). In addition, the expression of ET-1 and PAI-1 mRNA were go up significantly in a both time-dependent and dose-dependent manner(P<0.05),respectively.Conclusion:Elevated TSH can promote endothelial dysfunction and development of atherosclerosis.