Enhanced cell survival and diminished apoptotic response to simulated ischemia-reperfusion in H9c2 cells by magnetic field preconditioning

Apoptosis. 2012 Nov;17(11):1182-96. doi: 10.1007/s10495-012-0747-9.


The potential for 60 Hz magnetic field (MF) preconditioning to protect heart-derived, H9c2 cultures from damage by simulated ischemia and reperfusion (I-R) was examined. The most effective MF exposure conditions (120 μT, 4-8 h) increased cell survival by 40-50 % over that seen with I-R alone. Potential targets of MF preconditioning were assessed by investigating the apoptosis-related drop in Bcl-2 levels and elevation of the specific activities of caspases 3, 8 and 9 produced by I-R. In response to MF exposure Bcl-2 levels rose 2 to 2.6-fold, and caspase specific activities fell 51-72 % from the values seen after I-R alone. Levels of Hsp's 25, 32 and 72 were examined in response to the MF, but showed little-to-no elevation beyond that produced by I-R. However, MF preconditioning produced a 77 % decrease in the I-R-induced translocation of phosphorylated Hsp25 (Hsp25-P) from the cytosolic to the nuclear-cytoskeletal cell fraction. This might protect by maintaining active Hsp25-P in the cytosol to function as a chaperone or to bind cytochrome c. Blocking Hsp25 phosphorylation with SB203580, an inhibitor of p38 MAPK, resulted in increases of 64 and 80 % in the respective specific activities of caspases 3 and 9 in cells subjected to I-R, and eliminated the MF-induced reduction in caspase 3 activity.

MeSH terms

  • Animals
  • Apoptosis* / drug effects
  • Caspases / metabolism
  • Cell Line
  • Cell Nucleus / drug effects
  • Cell Nucleus / metabolism
  • Cell Survival / drug effects
  • Cytosol / metabolism
  • Fluorescent Antibody Technique
  • HSP27 Heat-Shock Proteins / metabolism
  • HSP72 Heat-Shock Proteins / metabolism
  • Heme Oxygenase (Decyclizing) / metabolism
  • Imidazoles / pharmacology
  • Ischemic Preconditioning*
  • Magnetic Fields*
  • Myocardial Reperfusion Injury / enzymology
  • Myocardial Reperfusion Injury / pathology*
  • Phosphorylation / drug effects
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Pyridines / pharmacology
  • Rats
  • Stress, Physiological / drug effects


  • HSP27 Heat-Shock Proteins
  • HSP72 Heat-Shock Proteins
  • Hspb1 protein, rat
  • Imidazoles
  • Proto-Oncogene Proteins c-bcl-2
  • Pyridines
  • Heme Oxygenase (Decyclizing)
  • Hmox1 protein, rat
  • Caspases
  • SB 203580