Effect of thyrotropin on nitric oxide synthase in human microvascular endothelial cells and its mechanism

Objective To investigate the effect of thyroid stimulating hormone (TSH) on the expression of endothelial nitric oxide synthase (eNOS) and its mechanism in human microvascular endothelial cells (HMEC-1) in vitro culture. Methods Different concentrations of TSH (0, 10, 50 mIU/ml) were used to intervene HMEC-1. The expression of eNOS mRNA was detected with quantitative polymerase chain reaction (qPCR) method. The protein expressions of eNOS, phosphorylated protein kinase B (p-AKT), protein kinase B (AKT), phosphorylated extracellular signal-regulated kinase (P-ERK), and extracellular signal-regulated kinase (ERK) were determined with Western Blot. Results ⑴ The expression level of eNOS was significantly decreased by TSH in dose-dependent manner (P<0.05). ⑵ TSH could promote the phosphorylation of AKT and ERK (P<0.05). Conclusions Thyroid-stimulating hormone may inhibit the expression of nitric oxide synthase in human microvascular endothelial cells by activating AKT and ERK signaling pathways. Key words: Thyrotropin/AD; Endothelial cells/DE/ME; Nitric oxide synthase/ME