Passive Ca(2+) overload in H9c2 cardiac myoblasts: assessment of cellular damage and cytosolic Ca(2+) transients

Arch Biochem Biophys. 2011 Aug 15;512(2):175-82. doi: 10.1016/j.abb.2011.05.019. Epub 2011 Jun 12.

Abstract

Increase of resting Ca(2+) levels and amplitude of vasopressin-induced Ca(2+) transients were observed when cells in serum-free medium were exposed to 5mM Ca(2+) for 2h. Small effect on cell viability was also observed. A rapid cytotoxic effect was developed in the presence of 10mM Ca(2+) and absence of serum. However, cells exposed to 10mM Ca(2+) in the presence of serum were protected from damage for at least 2days. Resting Ca(2+) levels and cytosolic Ca(2+) transients in serum-containing medium with 10mM Ca(2+) displayed lower increases and a tendency to recover control values. When serum was absent, cells preincubated with 10mM Ca(2+) were more sensitive to thapsigargin-induced damage than cells preincubated with lower Ca(2+). The sensitivity was similar when serum was present. Tolerance to high Ca(2+) in the presence of serum was linked to potentiation of the mitochondrial Ca(2+) entry to decrease the sarcoplasmic reticulum Ca(2+) overload.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Calcium / metabolism*
  • Calcium / pharmacology
  • Calcium Signaling / drug effects
  • Calcium Signaling / physiology
  • Cell Line
  • Cell Proliferation / drug effects
  • Culture Media
  • Culture Media, Serum-Free
  • Cytosol / drug effects
  • Cytosol / metabolism
  • Mitochondria, Heart / drug effects
  • Mitochondria, Heart / metabolism
  • Models, Cardiovascular
  • Myoblasts, Cardiac / drug effects
  • Myoblasts, Cardiac / metabolism*
  • Myoblasts, Cardiac / pathology
  • Rats
  • Sarcolemma / drug effects
  • Sarcolemma / metabolism
  • Sarcoplasmic Reticulum / drug effects
  • Sarcoplasmic Reticulum / metabolism
  • Thapsigargin / toxicity

Substances

  • Culture Media
  • Culture Media, Serum-Free
  • Thapsigargin
  • Calcium