Characterization of gene expression profile associated with energy restriction-induced cold tolerance of heart

Hypothermia is known to be a common feature of energy restriction (ER) and essential for a life-prolonging effect of ER. The heart is sensitive to hypothermia, but the heart in ER mice acquires some adaptation to hypothermia. The aim of the present study was to characterize the gene expression profile associated with ER-induced cold resistance of heart. We analyzed the expression of heart mRNA from ER (200 kJ/week) or control (400 kJ/week) B6 11-month-old male mice using cDNA array membranes including 588 genes. Eighty-eight out of 588 genes were expressed in the heart. mRNAs increased by ER were glutathion S-transferase Mu1, transcriptional factor 1 for heat shock gene (HSF1), and fetal myosin alkali light chain genes. mRNA decreased by ER were seven genes in four categories: (1). cell cycle or apoptosis-related proteins (cyclin G and nucleoside diphosphate kinase B); (2). stress response proteins (oxidative stress-induced protein); (3). DNA repair proteins (protein involved in DNA double-strand break repair, Rad23 UV excision repair protein homologue and ubiquitin-conjugating enzyme); and (4). cell-surface antigens (lamimin receptor 1). These data suggest that the heart of ER mice adapts to hypothermia involving heat shock proteins and their transcriptional factors and by changing structure and property of myofibrils. It is also suggested that ER induces protection against oxidative stress and inhibits cell proliferation of "nonmuscle cells" in the heart. Gene expression analysis using cDNA array was useful for screening genes associated with ER-induced cold adaptation.