Cardiac genomic response following preconditioning stimulus.
This review focuses on the genomic response following a preconditioning stimulus. Initial studies demonstrated that classical ischemic preconditioning mediated by cyclic episodes of short durations of reversible ischemia and reperfusion could result in the reprogramming of gene expression. Some of these genes are translated into proteins during the late preconditioning or so-called "second window of protection". Subsequent studies determined a unique similarity of the expressed gene profiles between diverse varieties of preconditioning including ischemic/hypoxic, heat shock, and oxidative stress. The most common genes that are expressed by virtually any kind of stress conditioning include antioxidants like superoxide dismutase, glutathione peroxidase and heme oxygenase and heat shock proteins such as HSP70. At a later date, differential display and subtractive hybridization techniques revealed the identities of many other genes including those belonging to mitochondrial respiratory chain such as ATPases. More recently, gene array profiles using gene chips determined several other genes triggered by preconditioning including the mitochondrial genes. The results of the studies present in the literature clearly indicate the existence of a strong resemblance between the patterns of gene expression profiles induced by diverse preconditioning stimuli, oxidative stress being situated at the cross-roads of all forms of the stresses. Redox signaling appears to be responsible for the conversion of the ischemia/reperfusion-induced "death signal" into preconditioning-mediated "survival signal".
Cardiovascular Research Center, University of Connecticut School of Medicine, Farmington, Connecticut, CT 06030-1110, USA. DDAS@NEURON.UCHC.EDU
Dipak K
DK
Das
Nilanjana
N
Maulik
D000818:Animals; D015687:Cell Hypoxia; D005786:Gene Expression Regulation; D006360:Heat-Shock Proteins / Q000235:genetics* / Q000378:metabolism; D006801:Humans; D019157:Ischemic Preconditioning, Myocardial; D009203:Myocardial Infarction / Q000235:genetics*; D009206:Myocardium / Q000378:metabolism*; D017382:Reactive Oxygen Species / Q000378:metabolism
D006360:Heat-Shock Proteins; D017382:Reactive Oxygen Species