Caveolin‑1 modulates hypertensive vascular remodeling via regulation of the Notch pathway.

Abstract

Hypertension is one of the critical risk factors of cerebrovascular disease. Caveolin-1 (Cav-1) has been suggested to be involved in the development of hypertension; however, the underlying mechanism remains largely unknown. Therefore, the present study aimed to investigate the mechanism underlying Cav-1 in hypertension. In the present study, the hypertension model was induced by infusion of angiotensin II (Ang-II) in rats. Cell Counting Kit-8 assay was used to detect the viability of human umbilical vein endothelial cells (HUVECs). Flow cytometry was used to determine the apoptosis of HUVECs. Transmission electron microscopy was utilized to address the thickness of the vessel walls. Reverse transcription-quantitative PCR, western blotting and immunofluorescence staining were used to assess the mechanism of cav-1/Notch1 involved in hypertensive vascular remodeling. In the present study, an Ang-II-induced hypertension model was successfully established in rats. With this model, it was found that the expression levels of cav-1 and Notch1 were significantly increased in brain tissues in the hypertension group compared with the sham-operated group. In cultured HUVECs, knockdown of cav-1 regulated Ang-II-induced HUVEC viability and apoptosis, and modulated hypertensive vascular remodeling, which was mediated by the Notch pathway. The data of the present study demonstrated that the cav-1/Notch signaling plays an important role in the regulation of Ang-II-induced hypertension and vascular remodeling.