title: Enhanced cell survival and diminished apoptotic response to simulated ischemia-reperfusion in H9c2 cells by magnetic field preconditioning.
abstract: 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.
authors.affiliation: Department of Biology, The Catholic University of America Cardinal Station, Washington, DC 20064, USA.
authors.forename: Mani V
authors.initials: MV
authors.lastname: Kurian
authors.forename: Lanette
authors.initials: L
authors.lastname: Hamilton
authors.forename: James
authors.initials: J
authors.lastname: Keeven
authors.forename: Patrick
authors.initials: P
authors.lastname: Mehl
authors.forename: James M
authors.initials: JM
authors.lastname: Mullins
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D020169:Caspases / Q000378:metabolism; D002460:Cell Line; D002467:Cell Nucleus / Q000187:drug effects / Q000378:metabolism; D002470:Cell Survival / Q000187:drug effects; D003600:Cytosol / Q000378:metabolism; D005455:Fluorescent Antibody Technique; D055551:HSP27 Heat-Shock Proteins / Q000378:metabolism; D050884:HSP72 Heat-Shock Proteins / Q000378:metabolism; D006419:Heme Oxygenase (Decyclizing) / Q000378:metabolism; D007093:Imidazoles / Q000494:pharmacology; D019194:Ischemic Preconditioning; D060526:Magnetic Fields; D015428:Myocardial Reperfusion Injury / Q000201:enzymology / Q000473:pathology*; D010766:Phosphorylation / Q000187:drug effects; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D011725:Pyridines / Q000494:pharmacology; D051381:Rats; D013312:Stress, Physiological / Q000187:drug effects
chemical_list: D055551:HSP27 Heat-Shock Proteins; D050884:HSP72 Heat-Shock Proteins; C486114:Hspb1 protein, rat; D007093:Imidazoles; D019253:Proto-Oncogene Proteins c-bcl-2; D011725:Pyridines; D006419:Heme Oxygenase (Decyclizing); C491523:Hmox1 protein, rat; D020169:Caspases; C093642:SB 203580