Copyright © 2006, European Society of Cardiology
Cardiac genomic response following preconditioning stimulus
Cardiovascular Research Center, University of Connecticut School of Medicine, Farmington, Connecticut, CT 06030-1110, USA
* Corresponding author. Tel.: +1 860 679 3687; fax: +1 860 679 4606. Email address: DDAS{at}NEURON.UCHC.EDU
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".
KEYWORDS Preconditioning; Second window of protection; Gene expression; Oxidative stress; Redox signaling; Heat shock protein; Ischemia; Hypoxia
Time for primary review 13 days
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