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Articles in PresS, published online ahead of print November 8, 2001
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00591.2001
Submitted on July 5, 2001
Accepted on November 7, 2001
1 Cardiovascular Medicine, Kyoto University Hospital, Kyoto, Kyoto, Japan
2 Molecular Oncology, Genentech, Inc., South San Francisco, CA, USA
* To whom correspondence should be addressed. E-mail: taoyama{at}kuhp.kyoto-u.ac.jp.
Cardiotrophin-1 (CT-1) stimulates longitudinal myocardial cell hypertrophy. We examined the expression of CT-1, leukemia inhibitory factor (LIF) and gp130 by competitive RT-PCR and Western blotting in Dahl salt-sensitive (DS) rats with a high-salt diet, which showed a distinct transition from left ventricular hypertrophy (LVH) to congestive heart failure (CHF). The expression levels of CT-1 mRNA and protein were significantly increased at the CHF stage compared with the LVH stage and age-matched Dahl salt-resistant (DR) rats (n=6 for each group). mRNA expression of LIF was not changed in the left ventricle at any stage by RT-PCR. gp130 mRNA and protein levels of DS rats at 11 and 17 weeks were significantly increased compared with age-matched DR rats. The isolated myocyte length of DS rats at 17 weeks was the longest among the 4 groups of rats. The left ventricular end-diastolic dimension (LVDd) of DS rats, determined by echocardiography, was significantly increased at the CHF stage. There was a significant correlation between the CT-1 protein level and LVDd. CT-1 may play a role in ventricular remodeling during transition from LVH to CHF in the rat hypertensive model.
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