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Chinese Journal of Clinical Pharmacology and Therapeutics ›› 2006, Vol. 11 ›› Issue (7): 789-796.

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Calcium caused calcium release causes a vascular smooth muscle cell line A10 cells apoptosis

WU Yu-lin, MA Bing-liang1 , DAI Xiao-ming, CHEN Lin-lin2   

  1. Department of Pharmacology, China Pharmaceutical University, Nanjing 210038, Jiangsu, China;1Department of Pharmacology, 2Department of Foreign Language, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China
  • Received:2005-09-13 Accepted:2006-01-15 Online:2006-07-26 Published:2020-10-30
  • About author:WU Yu-lin, male, PhD, associate professor, master di rector, majoring in cardiovascular pharmacology.Tel:025-85230873 E-mail:wylcpu@yahoo.com.cn

Abstract: AIM: To investigate the apoptosis of a vascular smooth muscle cell line A10 caused by mild K+depolarization.METHODS: Apoptosis was evaluated by nuclear staining, DNA fragmentation gel electrophoresis and propidium iodide-stained flow cytometry.Mitochondrial transmembrane potential (Δψm) was measured by flow cytometry.RESULTS: K+depolarization caused dose correlated A10 cells apoptosis; nifedipine, BAPTA AM, ryanodine inhibited the cytotoxic effect of K+completely.The combination use of nifedipine and cyclosporin A made it clear that mitochondria was involved in the apoptosis of A10 cells, and Δψm measurement further confirmed this speculation; A10 apoptosis caused by K+depolarization was not influenced by heparin or Zn2+, a effectivecapacitative calcium entry(CCE) blocker.CONCLUSION: Ca2+entry through voltage-dependent ca channels increases intracytoplasm Ca2+, then triggers furtherCa2+release from endoplasmic reticulum via ryanodine receptor, and the microdomains of elevated intracytoplasmCa2+are sensed by adjacent mitochondria, which ultimately lead to cell apoptosis.

Key words: vascular smooth muscle cell, apoptosis, calcium release, ryanodine, mitochondria

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