Ca2+ channel blockers verapamil and nifedipine inhibit apoptosis induced by 25-hydroxycholesterol in human aortic smooth muscle cells.

摘要: We have characterized the death of human aortic smooth muscle cells induced by 25-hydroxycholesterol, an oxidation product cholesterol. Chromatin condensation characteristic apoptosis was observed enzymatic (TUNEL) staining chromatin, and electron microscopy. Fourteen percent treated with 5 microg/ml 25-hydroxycholesterol for 24 h displayed chromatin degradation as determined positive TUNEL staining. Addition TNF alpha (10 ng/ml) IFN gamma (20 increased proportion to 30%, whereas cytokines alone were without effect. After 48 h, 40% positive, 21% condensation. Oligonucleosomal DNA fragmentation typical demonstrated agarose gel electrophoresis. Furthermore, activation ICE-like protease caspase 3 (CPP32) in 25-hydroxycholesterol. Ca2+ entry blockers verapamil or nifedipine culture medium inhibited more than 70% reduced cytotoxicity, while removal from 42%. Within a few minutes after addition, intracellular oscillations frequency approximately 0.3-0.4 min(-1). Thus it appears that influx through plasma membrane channels is important signal oxysterol-induced apoptosis. enhanced cytotoxicity resulted higher apoptotic cells, suggesting inflammatory can increase lipid products.