Gene expression profiling of the aging mouse cardiac myocytes

被引:66
作者
Bodyak, N
Kang, PM
Hiromura, M
Sulijoadikusumo, I
Horikoshi, N
Khrapko, K
Usheva, A [1 ]
机构
[1] Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Dept Med,Div Endocrinol, Boston, MA 02215 USA
[2] Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Dept Med,Div Cardiol, Boston, MA 02215 USA
[3] Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Dept Med,Div Gerontol, Boston, MA 02215 USA
[4] Washington Univ, Sch Med, Dept Radiat Oncol, St Louis, MO USA
关键词
D O I
10.1093/nar/gkf497
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:3788 / 3794
页数:7
相关论文
共 37 条
[1]   The sarcoplasmic reticulum Ca2+-ATPase (SERCA2) gene promoter activity is decreased in response to severe left ventricular pressure-overload hypertrophy in rat hearts [J].
Aoyagi, T ;
Yonekura, K ;
Eto, Y ;
Matsumoto, A ;
Yokoyama, I ;
Sugiura, S ;
Momomura, S ;
Hirata, Y ;
Baker, DL ;
Periasamy, M .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 1999, 31 (04) :919-926
[2]   INDUCTION OF HEME OXYGENASE-1 GENE-EXPRESSION BY LIPOPOLYSACCHARIDE IS MEDIATED BY AP-1 ACTIVATION [J].
CAMHI, SL ;
ALAM, J ;
OTTERBEIN, L ;
SYLVESTER, SL ;
CHOI, AMK .
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 1995, 13 (04) :387-398
[3]   Heme oxygenase-1: Function, regulation, and implication of a novel stress-inducible protein in oxidant-induced lung injury [J].
Choi, AMK ;
Alam, J .
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 1996, 15 (01) :9-19
[4]   Heme oxygenase-1 protects the heart [J].
Choi, AMK .
CIRCULATION RESEARCH, 2001, 89 (02) :105-107
[5]   The co-chaperone CHIP regulates protein triage decisions mediated by heat-shock proteins [J].
Connell, P ;
Ballinger, CA ;
Jiang, JH ;
Wu, YX ;
Thompson, LJ ;
Höhfeld, J ;
Patterson, C .
NATURE CELL BIOLOGY, 2001, 3 (01) :93-96
[6]   THE CARDIOMYOPATHY OF DUCHENNES MUSCULAR-DYSTROPHY AND THE FUNCTION OF DYSTROPHIN [J].
CZINER, DG ;
LEVIN, RI .
MEDICAL HYPOTHESES, 1993, 40 (03) :169-173
[7]   Dystrophin-deficient cardiomyocytes are abnormally vulnerable to mechanical stress-induced contractile failure and injury [J].
Danialou, G ;
Comtois, AS ;
Dudley, R ;
Karpati, G ;
Vincent, GV ;
Des Rosiers, C ;
Petrof, BJ .
FASEB JOURNAL, 2001, 15 (07) :1655-+
[8]   The creatine kinase system is essential for optimal refill of the sarcoplasmic reticulum Ca2+ store in skeletal muscle [J].
de Groof, AJC ;
Fransen, JAM ;
Errington, RJ ;
Willems, PHGM ;
Wieringa, B ;
Koopman, WJH .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (07) :5275-5284
[9]   THE MOUSE PLASMA-MEMBRANE CA2+ PUMP ISOFORM-1 PROMOTER - CLONING AND CHARACTERIZATION [J].
DU, YS ;
CARLOCK, L ;
KUO, TH .
ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS, 1995, 316 (01) :302-310
[10]   X-linked dilated cardiomyopathy and the dystrophin gene [J].
Ferlini, A ;
Sewry, C ;
Melis, MA ;
Mateddu, A ;
Muntoni, F .
NEUROMUSCULAR DISORDERS, 1999, 9 (05) :339-346