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Hypertension impairs the morphological and functional integrity of circulation. Previous research has shown that the loss of endothelial cells (ECs) is a common event in many cardiovascular diseases. p120 catenin (p120ctn) plays an important role in the regulation of inflammatory responses in ECs. However, the functional significance of p120ctn in angiotensin II (AngII)-induced apoptosis of human umbilical vein endothelial cells (HUVECs) had not previously received much scholarly attention. In the present study, using western blot analysis and RT-PCR, we found that AngII-induced cell apoptosis was correlated with a significant decrease in p120ctn expression. The effect of AngII on cell viability was measured by CCK-8 assay. Knockdown of p120ctn with small hairpin RNA (shRNA) increased AngII-induced apoptosis of HUVECs, as demonstrated by Annexin V/PI staining and flow cytometric analysis. Knockdown of p120ctn with shRNA also increased cytochrome c release into the cytoplasm, and cleaved caspase-3 and -9 protein expression. These were accompanied by a decrease in the Bcl-2/Bax ratio (Bcl-2 and Bax protein expression were measured by western blot analysis), and in mitochondrial membrane potential, as measured using JC-1. Overexpression of p120ctn with adenovirus produced opposite effects. In the present study, we demonstrated that p120ctn attenuated AngII‑induced apoptosis of HUVECs through the mitochondria-dependent pathway, suggesting that p120ctn plays a critical role in protecting ECs against apoptosis during hypertension.

p120 catenin attenuates the angiotensin II-induced apoptosis of human umbilical vein endothelial cells by suppressing the mitochondrial pathway