1999 Fiscal Year Final Research Report Summary
The role of Candiotrophin-1 and its receptoi component, rpbi, in the heart.
| Project/Area Number |
10670647
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
AOYAMA Takesh Kyoto University, Candiorasculan Medicine, Instructor, 医学研究科, 助手 (30222491)
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| Project Period (FY) |
1998 – 1999
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| Keywords | myocardial infarction / rentricular remodeling / cardiotrophin-1 / gp-130 |
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| Research Abstract |
Cardiotrophin-1 (CT-1) is a potent cytokine that stimulates the assembly of sarcomeric units in series in cardiomyocytes through gp130 signaling, resulting in myocardial cell hypertrophy. We examined the role of CT-1 and gp130 system in the two rat models of congestive heart failure. TO clarify the role of CT-1 and the gp130-signaling pathway during ventricular remodeling after myocardial infarction. we examined the expression of CT-1 and gp130 in a rat model of myocardial infarction. All animals developed large myocardial infarctions and progressive left ventricular dilatation and inadequate hypertrophy of the surviving myocardium were confirmed by echocardiography. CT-1 and gp130 mRNA levels were determined by semiquantitative RT-PCR followed by Southern blotting. The densitometric analysis of the Southern blots revealed a significant increase in CT-1 and gp130 mRNA levels compared with those of the sham-operated rats at 1, 3, 7, 14, 28 and 56 days post-infarct in the infarct area, t
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he ventricular septum and right ventricle. The protein levels of CT- and gp130, determined by Western blot analysis, were significantly increased compared to those of sham-operated rats, and peaked in the acute stage and declined thereafter in the three regions described above. Immunohistochemical staining showed that CT-1 and gp130-immunoreactivities were detected in cardiomyocytes and fibroblast-like cells and that the intensity of staining was increased at 7days post-infarct compared with that in sham-operated rats. An augmented CT-1 and gp130 system thus seems to play an important role during ventricular remodeling after myocardial infarction. We also determined the expression levels of CT-1 and gp130 during the transition from cardiac hypertrophy to heart failure using Dah1-salt-sensitive rats with hypertension. CT-1 expression was increased in the stage of heart failure, in which we confirmed the assembly of sarcomeric units in series. Thus, CT-1 contributes to the ventricular dilatation by elongating cardiomyocytes. These findings in the two heart failure models strongly suggest that CT-1 plays a central role in the ventricular dilatation in heart failure. Less
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Research Products
(9 results)
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[Publications] Eiji Shinoda, Yoshiki Yui, Ryuichi Hattori, Misaki Tanaka, Inoue Reiko, Takeshi Aoyama, Yoshihito Takimoto, Youji Mitsui, Kaoru Miyahara, Yutaka Shizuta, Shigetaka Sasayama.: "Tissue factor inhibitor-2 is a novel mitogen for vascular smooth muscle cells"J. Biol. Chem. Vol.274. 5379-5384 (1999)
Description
「研究成果報告書概要(欧文)」より
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