title: Ischemic but not mechanical preconditioning attenuates ischemia/reperfusion induced myocardial apoptosis in anaesthetized rabbits: the role of Bcl-2 family proteins and ERK1/2.
abstract: OBJECTIVE
  Recent studies suggest that ischemic preconditioning (IPC) inhibits myocardial apoptosis after ischemia and reperfusion. This study aimed first, to examine whether short mechanical stretch with acute pressure overload (MPC), which has been shown to reduce infarct size after ischemia/reperfusion, mimics IPC in attenuating myocardial apoptosis and second, to evaluate whether induced cardioprotection involves modulation of the expression of the Bcl-2 family proteins and phosphorylation of prosurvival kinases.
  
  
  RESULTS
  A model of anaesthetized rabbit was used and the preconditioning protocol included one cycle of short ischemia/reperfusion, or short mechanical stretch with acute pressure overload. Preconditioning stimuli were equally effective in reducing the infarct size, determined after 4 h reperfusion. However, IPC but not MPC attenuated myocardial apoptosis. IPC restored the decreased expression of Bcl-2 and Bcl-xL observed in hearts subjected to ischemia and reperfusion only. Bax levels were not different among the groups. ERK1/2 were activated during reperfusion in both IPC and MPC groups.
  
  
  CONCLUSIONS
  The data provide further evidence that apoptosis and necrosis contribute independently to infarct size after ischemia and reperfusion. Inhibition of the myocardial apoptotic processes by IPC may involve modulation of the expression of anti-apoptotic proteins, Bcl-2 and Bcl-xL. ERK1/2 may be involved in the inhibition of both apoptosis and necrosis.
authors.affiliation: Laboratory of Animal Physiology, Department of Zoology, School of Biology, Aristotle University of Thessaloniki, Thessaloniki, 54124, Greece. lazou@bio.auth.gr
authors.forename: Antigone
authors.initials: A
authors.lastname: Lazou
authors.forename: E K
authors.initials: EK
authors.lastname: Iliodromitis
authors.forename: D
authors.initials: D
authors.lastname: Cieslak
authors.forename: K
authors.initials: K
authors.lastname: Voskarides
authors.forename: S
authors.initials: S
authors.lastname: Mousikos
authors.forename: E
authors.initials: E
authors.lastname: Bofilis
authors.forename: D T
authors.initials: DT
authors.lastname: Kremastinos
mesh_terms: D000758:Anesthesia; D000818:Animals; D017209:Apoptosis; D053148:Caspase 3 / Q000378:metabolism; D053938:DNA Fragmentation; D004789:Enzyme Activation; D019157:Ischemic Preconditioning, Myocardial / Q000379:methods*; D008297:Male; D019950:Mitogen-Activated Protein Kinase 1 / Q000378:metabolism*; D048052:Mitogen-Activated Protein Kinase 3 / Q000378:metabolism*; D009203:Myocardial Infarction / Q000473:pathology; D015428:Myocardial Reperfusion Injury / Q000139:chemically induced* / Q000473:pathology; D032383:Myocytes, Cardiac / Q000166:cytology*; D010766:Phosphorylation; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism*; D011817:Rabbits; D051028:bcl-2-Associated X Protein / Q000378:metabolism; D051020:bcl-X Protein / Q000378:metabolism
chemical_list: D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein; D051020:bcl-X Protein; D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3; D053148:Caspase 3