title: Gene expression profiling of exercise-induced cardiac hypertrophy in rats.
abstract: OBJECTIVE
  Exercise training causes physiological cardiac hypertrophy, which acts to enhance cardiac function during exercise. However, the underlying molecular mechanisms are unclear. We investigated gene expression profile of exercise training-induced cardiac hypertrophy using left ventricle (LV) excised from exercise-trained and sedentary control rats (12-week old).
  
  
  METHODS
  Rats in the training group exercised on a treadmill for 8-week.
  
  
  RESULTS
  Left ventricular mass index and wall thickness in the exercise-trained group were significantly greater than that in the control group, indicating that the trained rats developed cardiac hypertrophy. Of the 3800 genes analysed in the microarray analyses, a total of 75 relevant genes (upregulation of 33 genes and downregulation of 42 genes) displayed alterations with exercise training. Among these genes, we focused on glycogen synthase kinase (GSK)-3beta, calcineurin-inhibitor (Cain), and endothelin (ET)-1 for their implicated roles in pathological cardiac hypertrophy, and confirmed the results of microarray analysis at mRNA and protein/peptide levels using quantitative PCR, Western blot, and EIA analyses. The gene expression of GSK-3beta decreased significantly and those of Cain and ET-1 increased significantly with exercise training. Furthermore, LV mass index was significantly correlated with GSK-3beta protein activity (r = -0.70, P < 0.01) and tissue ET-1 concentration (r = 0.52, P < 0.05). There were no changes in gene expressions in brain natriuretic peptide (BNP), angiotensin-correcting enzyme (ACE), interleukin-6, and vascular cell adhesion molecule (VCAM)-1.
  
  
  CONCLUSIONS
  These findings suggest that physiological and pathological LV hypertrophy may share some of the same molecular mechanisms in inducing LV hypertrophy (e.g. GSK-3beta, Cain, and ET-1) and that other genes (e.g. BNP, ACE) may differentiate physiological from pathological LV hypertrophy.
authors.affiliation: Institute of Health and Sport Sciences, University of Tsukuba, Tsukuba, Ibaraki, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Iemitsu
authors.forename: S
authors.initials: S
authors.lastname: Maeda
authors.forename: T
authors.initials: T
authors.lastname: Miyauchi
authors.forename: M
authors.initials: M
authors.lastname: Matsuda
authors.forename: H
authors.initials: H
authors.lastname: Tanaka
mesh_terms: D000222:Adaptation, Physiological; D000818:Animals; D051017:Apoptosis Regulatory Proteins; D015153:Blotting, Western; D006332:Cardiomegaly / Q000235:genetics*; D002352:Carrier Proteins / Q000032:analysis / Q000235:genetics; D019332:Endothelin-1 / Q000032:analysis / Q000235:genetics; D015870:Gene Expression; D020869:Gene Expression Profiling; D038362:Glycogen Synthase Kinase 3 / Q000032:analysis / Q000235:genetics; D000071679:Glycogen Synthase Kinase 3 beta; D006352:Heart Ventricles; D007124:Immunoenzyme Techniques; D008297:Male; D023421:Models, Animal; D020411:Oligonucleotide Array Sequence Analysis; D010805:Physical Conditioning, Animal; D051381:Rats; D017207:Rats, Sprague-Dawley; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D051017:Apoptosis Regulatory Proteins; C113573:Cabin1 protein, rat; D002352:Carrier Proteins; D019332:Endothelin-1; D000071679:Glycogen Synthase Kinase 3 beta; C000605508:Gsk3b protein, rat; D038362:Glycogen Synthase Kinase 3