DNA microarray analysis of in vivo progression mechanism of heart failure

Dahl salt-sensitive rats are genetically hypersensitive to sodium intake. When fed a high sodium diet, they develop systemic hypertension, followed by cardiac hypertrophy and finally heart failure within a few months. Therefore, Dahl rats represent a good model with which to study how heart failure...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2003-08, Vol.307 (4), p.771-777
Main Authors: Ueno, Shuichi, Ohki, Ruri, Hashimoto, Toru, Takizawa, Toshihiro, Takeuchi, Koichi, Yamashita, Yoshihiro, Ota, Jun, Choi, Young Lim, Wada, Tomoaki, Koinuma, Koji, Yamamoto, Keiji, Ikeda, Uichi, Shimada, Kazuyuki, Mano, Hiroyuki
Format: Article
Language:English
Subjects:
Animals
Cardiomegaly - etiology
Cardiomegaly - genetics
Cardiomegaly - metabolism
Cardiomegaly - pathology
Cells, Cultured
Dahl salt-sensitive rat
DBP
Disease Progression
DNA microarray
Down-Regulation
Gene Expression Profiling
Heart failure
Heart Failure - etiology
Heart Failure - genetics
Heart Failure - metabolism
Heart Failure - pathology
Hypertension
Myocytes, Cardiac - metabolism
Oligonucleotide Array Sequence Analysis
Rats
Rats, Inbred Dahl
Reverse Transcriptase Polymerase Chain Reaction
Transcription, Genetic
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Summary:Dahl salt-sensitive rats are genetically hypersensitive to sodium intake. When fed a high sodium diet, they develop systemic hypertension, followed by cardiac hypertrophy and finally heart failure within a few months. Therefore, Dahl rats represent a good model with which to study how heart failure is developed in vivo. By using DNA microarray, we here monitored the transcriptome of >8000 genes in the left ventricular muscles of Dahl rats during the course of cardiovascular damage. Expression of the atrial natriuretic peptide gene was, for instance, induced in myocytes by sodium overload and further enhanced even at the heart failure stage. Interestingly, expression of the gene for the D-binding protein, an apoptotic-related transcriptional factor, became decreased upon the transition to heart failure. To our best knowledge, this is the first report to describe the transcriptome of cardiac myocytes during the disease progression of heart failure.
ISSN:0006-291X
1090-2104
DOI:10.1016/S0006-291X(03)01252-X