No abstract

Background Androgens play an essential role in maintaining vascular hemostasis via the regulation of autophagy, but the underlying mechanisms remain unknown. Here we investigated the effects of androgen deficiency in a rat castration model and the effects of androgen treatment in human umbilical vein smooth muscle cells (HUVSMCs). Male Sprague–Dawley rats were divided into two groups: (A) control group, (B) castration group. The vasodilation and vasoconstriction effect of dihydrotestosterone (DHT) were detected on rat thoracic aortic rings. Transmission electron microscopy was used to determine the levels of autophagy. Masson’s trichrome staining, MTT assay and flow cytometry were performed to detect the levels of HUVSMC cell proliferation. Results Androgen deficiency led to significantly enhance in the vasoconstriction and reductions in the vasodilatation of rat thoracic aortic rings. Treatment with rapamycin or 3-MA attenuated and enhanced, respectively, the vasorelaxation effect of androgen deficiency. Autophagy was significantly increased in the endothelial cells and SMCs of the thoracic aortic rings of model rats. Moreover, androgen deficiency induced excessive proliferation of SMCs. Treatment of HUVMSCs with high concentrations of DHT increased the percentage of cells in G0/G1 phase and reduced the percentages of cells in the G2 phase and S phase. Conclusions It was concluded that vascular injury resulting from androgen deficiency is mediated, in part, by increased autophagy. By promoting SMCs proliferation, androgen deficiency results in alteration of the aortic structure and aggravates vascular injury. Androgen treatment can inhibit the excessive proliferation of SMCs.