Τίτλος:
Ischemic but not mechanical preconditioning attenuates ischemia/reperfusion induced myocardial apoptosis in anaesthetized rabbits: The role of Bcl-2 family proteins and ERK1/2
Γλώσσες Τεκμηρίου:
Αγγλικά
Περίληψη:
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. Methods and 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. © 2006 Springer Science + Business Media, LLC.
Συγγραφείς:
Lazou, A.
Iliodromitis, E.K.
Cieslak, D.
Voskarides, K.
Mousikos, S.
Bofilis, E.
Kremastinos, D.T.
Λέξεις-κλειδιά:
mitogen activated protein kinase 1; mitogen activated protein kinase 3; protein bcl 2; protein bcl xl, anesthesia; animal cell; animal experiment; animal model; animal tissue; apoptosis; article; cell death; controlled study; enzyme activation; gene expression; heart infarction size; heart muscle reperfusion; heart protection; inhibition kinetics; ischemic heart disease; ischemic preconditioning; male; mechanical stress; nonhuman; priority journal; protein phosphorylation; rabbit, Anesthesia; Animals; Apoptosis; bcl-2-Associated X Protein; bcl-X Protein; Caspase 3; DNA Fragmentation; Enzyme Activation; Ischemic Preconditioning, Myocardial; Male; Mitogen-Activated Protein Kinase 1; Mitogen-Activated Protein Kinase 3; Myocardial Infarction; Myocardial Reperfusion Injury; Myocytes, Cardiac; Phosphorylation; Proto-Oncogene Proteins c-bcl-2; Rabbits, Oryctolagus cuniculus
DOI:
10.1007/s10495-006-0292-5
