title: Genetic expression profiles during physiological and pathological cardiac hypertrophy and heart failure in rats.
abstract: Cardiac hypertrophy is a complex and nonhomogenous response to various stimuli. In this study, we used high-density oligonucleotide microarray to examine gene expression profiles during physiological hypertrophy, pathological hypertrophy, and heart failure in Dahl salt-sensitive rats. There were changes in 404/3,160 and 874/3,160 genes between physiological and pathological hypertrophy and the transition from hypertrophy to heart failure, respectively. There were increases in stress response genes (e.g., heat shock proteins) and inflammation-related genes (e.g., pancreatitis-associated protein and arachidonate 12-lipoxygenase) in pathological processes but not in physiological hypertrophy. Furthermore, atrial natriuretic factor and brain natriuretic protein showed distinctive changes that are very specific to different conditions. In addition, we used a resampling-based gene score-calculating method to define significantly altered gene clusters, based on Gene Ontology classification. It revealed significant alterations in genes involved in the apoptosis pathway during pathological hypertrophy, suggesting that the apoptosis pathway may play a role during the transition to heart failure. In addition, there were significant changes in glucose/insulin signaling, protein biosynthesis, and epidermal growth factor signaling during physiological hypertrophy but not during pathological hypertrophy.
authors.affiliation: Cardiovascular Division, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA.
authors.forename: Sek Won
authors.initials: SW
authors.lastname: Kong
authors.forename: Natalya
authors.initials: N
authors.lastname: Bodyak
authors.forename: Patrick
authors.initials: P
authors.lastname: Yue
authors.forename: Zhilin
authors.initials: Z
authors.lastname: Liu
authors.forename: Jeffrey
authors.initials: J
authors.lastname: Brown
authors.forename: Seigo
authors.initials: S
authors.lastname: Izumo
authors.forename: Peter M
authors.initials: PM
authors.lastname: Kang
mesh_terms: D000818:Animals; D017209:Apoptosis; D009320:Atrial Natriuretic Factor / Q000096:biosynthesis; D015152:Blotting, Northern; D006332:Cardiomegaly / Q000473:pathology*; D004452:Echocardiography; D004815:Epidermal Growth Factor / Q000378:metabolism; D020869:Gene Expression Profiling / Q000379:methods*; D005786:Gene Expression Regulation; D006333:Heart Failure / Q000473:pathology*; D006984:Hypertrophy; D007249:Inflammation; D007328:Insulin / Q000378:metabolism; D020097:Natriuretic Peptide, Brain / Q000096:biosynthesis; D020411:Oligonucleotide Array Sequence Analysis; D000073718:Pancreatitis-Associated Proteins; D010805:Physical Conditioning, Animal; D012313:RNA / Q000737:chemistry; D051381:Rats; D020303:Rats, Inbred Dahl; D015398:Signal Transduction
chemical_list: D007328:Insulin; D000073718:Pancreatitis-Associated Proteins; C000612141:REG3A protein, human; D020097:Natriuretic Peptide, Brain; D004815:Epidermal Growth Factor; D012313:RNA; D009320:Atrial Natriuretic Factor