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Nucleic Acids Research, 2002, Vol. 30, No. 17 3788-3794
© 2002 Oxford University Press

Gene expression profiling of the aging mouse cardiac myocytes

Natalya Bodyak, Peter M. Kang1, Makoto Hiromura, Indra Sulijoadikusumo, Nobuo Horikoshi3, Konstantin Khrapko2 and Anny Usheva*

Division of Endocrinology, 1 Division of Cardiology and 2 Division of Gerontology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA and 3 Washington University, School of Medicine, Department of Radiation Oncology, St Louis, MO, USA

*To whom correspondence should be addressed. Tel: +1 617 632 0522; Fax: +1 617 667 2927; Email: ausheva{at}caregroup.harvard.edu

Heart disease remains the most frequent cause of death in the general population with increasing incidence in the elderly population. The pathologic failure of the aging heart may be related to structural and functional alterations in cardiac muscle cells. However, the molecular mechanisms underlying the aging-related decline in cardiac muscle function are largely unknown. To provide the first analysis of cardiac aging at the level of gene expression, we established and compared cDNA libraries from apparently healthy young and aged mouse ventricular cardiac muscle cells. We report the identification of genes that exhibit aging-related changes of mRNA levels. Aging expression profiles in aged hearts indicate decreased cellular adaptation and protection against stress-induced injury together with the development of contractile dysfunction. The data suggest reduced activity of the mitochondrial electron transport system and reduced levels of cardiac-specific transcription regulators. The cardiomyocyte aging profile of gene expression displays similarities with known heart disorders. Genes whose mRNA levels change with aging in cardiomyocytes might profoundly affect pathological changes in the heart.


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