Abstract
Originalsprog | Engelsk |
---|---|
Tidsskrift | FEBS Journal |
Vol/bind | 272 |
Udgave nummer | 11 |
Sider (fra-til) | 2684-95 |
Antal sider | 11 |
ISSN | 1742-464X |
DOI | |
Status | Udgivet - 2005 |
Bibliografisk note
Keywords: Animals; Biological Markers; Blood Pressure; Fatty Acids; Gene Expression Profiling; Glucose; Heart Ventricles; Hypertrophy, Left Ventricular; Male; Myocardial Infarction; Oligonucleotide Array Sequence Analysis; Phenotype; Physical Conditioning, Animal; RNA, Messenger; Rats; Rats, WistarAdgang til dokumentet
Citationsformater
- APA
- Standard
- Harvard
- Vancouver
- Author
- BIBTEX
- RIS
Expression profiling reveals differences in metabolic gene expression between exercise-induced cardiac effects and maladaptive cardiac hypertrophy. / Strøm, Claes C; Aplin, Mark; Ploug, Thorkil; Christoffersen, Tue E H; Langfort, Jozef; Viese, Michael; Galbo, Henrik; Haunsø, Stig; Sheikh, Søren P.
I: FEBS Journal, Bind 272, Nr. 11, 2005, s. 2684-95.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review
}
TY - JOUR
T1 - Expression profiling reveals differences in metabolic gene expression between exercise-induced cardiac effects and maladaptive cardiac hypertrophy.
AU - Strøm, Claes C
AU - Aplin, Mark
AU - Ploug, Thorkil
AU - Christoffersen, Tue E H
AU - Langfort, Jozef
AU - Viese, Michael
AU - Galbo, Henrik
AU - Haunsø, Stig
AU - Sheikh, Søren P
N1 - Keywords: Animals; Biological Markers; Blood Pressure; Fatty Acids; Gene Expression Profiling; Glucose; Heart Ventricles; Hypertrophy, Left Ventricular; Male; Myocardial Infarction; Oligonucleotide Array Sequence Analysis; Phenotype; Physical Conditioning, Animal; RNA, Messenger; Rats; Rats, Wistar
PY - 2005
Y1 - 2005
N2 - While cardiac hypertrophy elicited by pathological stimuli eventually leads to cardiac dysfunction, exercise-induced hypertrophy does not. This suggests that a beneficial hypertrophic phenotype exists. In search of an underlying molecular substrate we used microarray technology to identify cardiac gene expression in response to exercise. Rats exercised for seven weeks on a treadmill were characterized by invasive blood pressure measurements and echocardiography. RNA was isolated from the left ventricle and analysed on DNA microarrays containing 8740 genes. Selected genes were analysed by quantitative PCR. The exercise program resulted in cardiac hypertrophy without impaired cardiac function. Principal component analysis identified an exercise-induced change in gene expression that was distinct from the program observed in maladaptive hypertrophy. Statistical analysis identified 267 upregulated genes and 62 downregulated genes in response to exercise. Expression changes in genes encoding extracellular matrix proteins, cytoskeletal elements, signalling factors and ribosomal proteins mimicked changes previously described in maladaptive hypertrophy. Our most striking observation was that expression changes of genes involved in beta-oxidation of fatty acids and glucose metabolism differentiate adaptive from maladaptive hypertrophy. Direct comparison to maladaptive hypertrophy was enabled by quantitative PCR of key metabolic enzymes including uncoupling protein 2 (UCP2) and fatty acid translocase (CD36). DNA microarray analysis of gene expression changes in exercise-induced cardiac hypertrophy suggests that a set of genes involved in fatty acid and glucose metabolism could be fundamental to the beneficial phenotype of exercise-induced hypertrophy, as these changes are absent or reversed in maladaptive hypertrophy.
AB - While cardiac hypertrophy elicited by pathological stimuli eventually leads to cardiac dysfunction, exercise-induced hypertrophy does not. This suggests that a beneficial hypertrophic phenotype exists. In search of an underlying molecular substrate we used microarray technology to identify cardiac gene expression in response to exercise. Rats exercised for seven weeks on a treadmill were characterized by invasive blood pressure measurements and echocardiography. RNA was isolated from the left ventricle and analysed on DNA microarrays containing 8740 genes. Selected genes were analysed by quantitative PCR. The exercise program resulted in cardiac hypertrophy without impaired cardiac function. Principal component analysis identified an exercise-induced change in gene expression that was distinct from the program observed in maladaptive hypertrophy. Statistical analysis identified 267 upregulated genes and 62 downregulated genes in response to exercise. Expression changes in genes encoding extracellular matrix proteins, cytoskeletal elements, signalling factors and ribosomal proteins mimicked changes previously described in maladaptive hypertrophy. Our most striking observation was that expression changes of genes involved in beta-oxidation of fatty acids and glucose metabolism differentiate adaptive from maladaptive hypertrophy. Direct comparison to maladaptive hypertrophy was enabled by quantitative PCR of key metabolic enzymes including uncoupling protein 2 (UCP2) and fatty acid translocase (CD36). DNA microarray analysis of gene expression changes in exercise-induced cardiac hypertrophy suggests that a set of genes involved in fatty acid and glucose metabolism could be fundamental to the beneficial phenotype of exercise-induced hypertrophy, as these changes are absent or reversed in maladaptive hypertrophy.
U2 - 10.1111/j.1742-4658.2005.04684.x
DO - 10.1111/j.1742-4658.2005.04684.x
M3 - Journal article
C2 - 15943803
VL - 272
SP - 2684
EP - 2695
JO - F E B S Journal
JF - F E B S Journal
SN - 1742-464X
IS - 11
ER -