Passive Ca2+ overload in H9c2 cardiac myoblasts: Assessment of cellular damage and cytosolic Ca2+ transients

被引:2
作者
Soler, Fernando [1 ]
Lax, Antonio [1 ,2 ]
Carmen Asensio, M. [2 ]
Pascual-Figal, Domingo [2 ]
Fernandez-Belda, Francisco [1 ]
机构
[1] Univ Murcia, Dept Bioquim & Biol Mol A, E-30071 Murcia, Spain
[2] Univ Murcia, Dept Med Interna Cardiol, Fac Med, Murcia 30120, Spain
关键词
Sarcoplasmic reticulum; Thapsigargin; Ca2+ overload; Ca2+ transient; Cell damage; H9c2; cell; ENDOPLASMIC-RETICULUM STRESS; SARCOPLASMIC-RETICULUM; CALCIUM; APOPTOSIS; DEATH; THAPSIGARGIN; OSCILLATIONS; HYPERTROPHY; CA2+-ATPASE; ACTIVATION;
D O I
10.1016/j.abb.2011.05.019
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Increase of resting Ca2+ levels and amplitude of vasopressin-induced Ca2+ transients were observed when cells in serum-free medium were exposed to 5 mM Ca2+ for 2 h. Small effect on cell viability was also observed. A rapid cytotoxic effect was developed in the presence of 10 mM Ca2+ and absence of serum. However, cells exposed to 10 mM Ca2+ in the presence of serum were protected from damage for at least 2 days. Resting Ca2+ levels and cytosolic Ca2+ transients in serum-containing medium with 10 mM Ca2+ displayed lower increases and a tendency to recover control values. When serum was absent, cells preincubated with 10 mM Ca2+ were more sensitive to thapsigargin-induced damage than cells preincubated with lower Ca2+. The sensitivity was similar when serum was present. Tolerance to high Ca2+ in the presence of serum was linked to potentiation of the mitochondrial Ca2+ entry to decrease the sarcoplasmic reticulum Ca2+ overload. (C) 2011 Elsevier Inc. All rights reserved.
引用
收藏
页码:175 / 182
页数:8
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