title: The signaling pathway of cardiotrophin-1 is not activated in hypertrophied ventricles of carnitine-deficient juvenile visceral steatosis (JVS) mice.
abstract: Cardiotrophin-1 (CT-1) is a novel cytokine which is involved in the growth and survival of cardiac cells. We examined whether CT-1 plays a role in the development of cardiac hypertrophy in carnitine-deficient juvenile visceral steatosis (JVS) mice. The CT-1 mRNA level was quantitatively measured by the competitive RT-PCR method. In contrast to other models including spontaneously hypertensive rats, CT-1 mRNA in the ventricles of JVS mice was comparable to the control at 5 days and was less than half the control value at 2 and 8 weeks when the ventricles of the JVS mice were highly hypertrophied. There were no significant differences in CT-1 mRNA levels in the lung, liver, kidney, small intestine and skeletal muscle between the JVS and control mice at 2 weeks. We did not find any difference between JVS and control mice at 2 weeks in the mRNA level of ventricular leukemia inhibitory factor (LIF) which binds to the same receptor as CT-1. Furthermore, almost no phosphorylated STAT3 (signal transducer and activator of transcription 3), downstream of the LIF receptor and the gp130 signaling subunit, was observed in the ventricles of JVS and control mice. These data show that the CT-1 signaling pathway does not play a significant role in the development of cardiac hypertrophy in JVS mice. Furthermore, we could not detect any differences in insulin-like growth factor I and II mRNA levels. All these data suggest distinct differences in the mechanisms of cardiac hypertrophy between JVS mice and other model animals.
authors.affiliation: Department of Biochemistry, Faculty of Medicine, Kagoshima University, Japan.
authors.forename: G
authors.initials: G
authors.lastname: Yoshida
authors.forename: M
authors.initials: M
authors.lastname: Horiuchi
authors.forename: K
authors.initials: K
authors.lastname: Kobayashi
authors.forename: M D
authors.initials: MD
authors.lastname: Jalil
authors.forename: M
authors.initials: M
authors.lastname: Iijima
authors.forename: S
authors.initials: S
authors.lastname: Hagihara
authors.forename: N
authors.initials: N
authors.lastname: Nagao
authors.forename: T
authors.initials: T
authors.lastname: Saheki
mesh_terms: D000818:Animals; D006332:Cardiomegaly / Q000378:metabolism*; D002331:Carnitine / Q000172:deficiency*; D016207:Cytokines / Q000235:genetics / Q000378:metabolism / Q000502:physiology*; D004268:DNA-Binding Proteins / Q000378:metabolism; D015870:Gene Expression; D006131:Growth Inhibitors / Q000235:genetics; D006352:Heart Ventricles / Q000378:metabolism*; D007334:Insulin-Like Growth Factor I / Q000235:genetics; D007335:Insulin-Like Growth Factor II / Q000235:genetics; D015850:Interleukin-6; D053605:Leukemia Inhibitory Factor; D008222:Lymphokines / Q000235:genetics; D051379:Mice; D008817:Mice, Mutant Strains; D010766:Phosphorylation; D050796:STAT3 Transcription Factor; D015398:Signal Transduction; D015534:Trans-Activators / Q000378:metabolism
chemical_list: D016207:Cytokines; D004268:DNA-Binding Proteins; D006131:Growth Inhibitors; D015850:Interleukin-6; D053605:Leukemia Inhibitory Factor; C507838:Lif protein, mouse; D008222:Lymphokines; D050796:STAT3 Transcription Factor; C494087:Stat3 protein, mouse; D015534:Trans-Activators; D007334:Insulin-Like Growth Factor I; D007335:Insulin-Like Growth Factor II; C092073:cardiotrophin 1; D002331:Carnitine