Analysis of Altered Gene Expression During Ischemic Preconditioning

Publisher Summary This chapter presents an analysis of altered gene expression during ischemic preconditioning. Cellular and molecular mechanisms of ischemic preconditioning (PC) leading to the myocardial adaptation to ischemia are based on the fact that enhancement of the endogenous cellular defense system provides each cell with new protein synthesis and, thereby the means to protect itself when it is more susceptible to injury. The ability of the cells to acclimate to their new environment is the integral driving force for the adaptive modification of the cells. Such adaptation involves a number of cellular and biochemical alterations, including metabolic homeostasis and reprogramming of gene expression. The precise mechanism of ischemic preconditioning is far from clear. It is believed that ischemic preconditioning occurs in two different steps: (1) early effect (short-term adaptation) triggered between seconds to minutes that is likely to be receptor-mediated and potentiated by the release of some endogenous compound(s) and may last up to several hours (ischemic preconditioning); and (2) late effect (long-term adaptation) that may occur after several hours and may last days to months. Multiple kinases involving tyrosine kinase-mitogen-activated protein (MAP) kinases-MAPKAP kinase 2 play a major role in ischemic preconditioning.