title: Increased expression of cardiotrophin-1 during ventricular remodeling in hypertensive rats.
abstract: 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 wk were significantly increased compared with age-matched DR rats. The isolated myocyte length of DS rats at 17 wk was the longest among the four groups of rats. The LV 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.
authors.affiliation: Department of Cardiovascular Medicine, Graduate School of Medicine, Kyoto University, Sakyo-ku, Kyoto 606-8507, Japan.
authors.forename: Yoshihito
authors.initials: Y
authors.lastname: Takimoto
authors.forename: Takeshi
authors.initials: T
authors.lastname: Aoyama
authors.forename: Yoshitaka
authors.initials: Y
authors.lastname: Iwanaga
authors.forename: Toshiaki
authors.initials: T
authors.lastname: Izumi
authors.forename: Yasuki
authors.initials: Y
authors.lastname: Kihara
authors.forename: Diane
authors.initials: D
authors.lastname: Pennica
authors.forename: Shigetake
authors.initials: S
authors.lastname: Sasayama
mesh_terms: D000818:Animals; D001794:Blood Pressure; D002455:Cell Division; D002478:Cells, Cultured; D058966:Contactins; D016207:Cytokines / Q000235:genetics*; D004195:Disease Models, Animal; D004452:Echocardiography; D005786:Gene Expression Regulation; D006131:Growth Inhibitors / Q000235:genetics; D006321:Heart / Q000502:physiology*; D006333:Heart Failure / Q000235:genetics / Q000503:physiopathology; D006352:Heart Ventricles; D006439:Hemodynamics / Q000502:physiology*; D017379:Hypertrophy, Left Ventricular / Q000235:genetics / Q000503:physiopathology; D015850:Interleukin-6; D053605:Leukemia Inhibitory Factor; D008222:Lymphokines / Q000235:genetics; D008297:Male; D009200:Myocardial Contraction; D009206:Myocardium / Q000378:metabolism*; D019006:Neural Cell Adhesion Molecules / Q000235:genetics; D051381:Rats; D020303:Rats, Inbred Dahl; D012044:Regression Analysis; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D058966:Contactins; D016207:Cytokines; D006131:Growth Inhibitors; D015850:Interleukin-6; D053605:Leukemia Inhibitory Factor; D008222:Lymphokines; D019006:Neural Cell Adhesion Molecules; C092073:cardiotrophin 1