ABSTRACT
Aim To investigate whether CTSB is involved in hypoxia-induced injury of cardiac microvascular endothelial cells.Methods A hypoxia-induced endothelial cell injury model was used.Cardiac microvascular endothelial cells were isolated from CTSB gene knockout mice.CTSB was overexpressed by adenovirus delivery system, and bafilomycin was used to block autophagy.ELISA was used to detect the release of inflammatory factors.Tunel staining was used to detect the number of cell apoptosis.caspase-3 kit was used to detect the activity of cell caspase-3.Cells were infected with LC3-GFP-mCherry double-labeled adenovirus todetect cell autophagy flow.Results CTSB gene knockout could significantly aggravate the inflammation and apoptosis of endothelial cells induced by hypoxia, and increased autophagy.Overexpression of CTSB reduced the inflammation and apoptosis of endothelial cells induced by hypoxia, and increased autophagy.But bafilomycin treatment could significantly offset the inhibitory effect of CTSB overexpression on cell inflammation and apoptosis and the protective effect on cell autophagy.Conclusions CTSB knockout aggravates inflammation and apoptosis induced by hypoxia in endothelial cells; while the overexpression of CTSB ameliorates endothelial cell injury induced by hypoxia.CTSB maintains normal autophagy degradation in endothelial cells.BAF blocks the protective effect of CTSB on endothelial cells by inhibiting autophagy degradation.