• Search Research Projects
  • Search Researchers
  • How to Use
  1. Back to project page

1992 Fiscal Year Final Research Report Summary

METHOD FOR MEASUREMENT OF CELL PROLIFERATION INHIBITING FACTOR IN HEART

Research Project

Project/Area Number 03557038
Research Category

Grant-in-Aid for Scientific Research (B).

Allocation TypeSingle-year Grants
Research Field Circulatory organs internal medicine
Research InstitutionHOKKAIDO UNIVERSITY

Principal Investigator

KAWAGUCHI Hideaki  HOKKAIDO UNIVERSITY, Medical Hospital, Instructor, 医学部附属病院, 助手 (70161297)

Co-Investigator(Kenkyū-buntansha) OIKAWA Tseneyuki  SASAKI INSTITUTION, MOLECULAR CELL BIOLOGY CHIEF RESEARCHER, 細胞遺伝子部, (研究開発担当)部長 (80150241)
Project Period (FY) 1991 – 1992
KeywordsCARDIOMYOPATHY / COLLAGEN / FIBROSIS / REMODELING / EXTRACELLULAR MATRIX
Research Abstract

Extensive fibrosis is remarkable in cardiomyopathy. The purpose of this study is to characterize the collagen, one of the chief elements of the extracellular matrix of hereditarycardiomyopathic hamsters, and to examine the participation of the collagen in the occurrence and the progression of the cardiomyopathy. BIO53.58(5,11,22 weeks) was used as the model of the dilated cardiomyopathy and BIO14.6 (20,30 weeks) was used as the model of the hypertrophic cardiomyopahty. F1b was used as the control. The collagen content was almost constant at any age in F1b, but increased with aging in BIO53.58 and BIO14.6. Type III collagen increased significantly in BIO53.58 at 11 weeks and BIO14.6 at 20 weeks. Type V collagen decreased significantly in BIO14.6 at 30 weeks. Aceticacid solubility of collagen decreased in BIO53.58 and BIO14.6 with the progression of the fibrosis, but not in F1b. Reducible crosslinks showed the tendency to decrease in BIO53.58 progressively. Histologicallythick collagen fiber increased in BIO53.58 and BIO14.6. These findings indicate that in the early phase of the cardiomyopathy the extracellular matrix of the myocardium has characteristics that of the immature tissues which are rich in type III collagen. In later phase, the matrix resembles that of hard tissues whose collagen is mainly of type Icollagen and have low solubility. It is considered that the increase of the thick collagen fiber combined firmly in heart may affect the diastolicand the systolic function in addition to the loss of the cardiac muscle fiber by the deg eneration and the necrosis.

  • Research Products

    (16 results)

All Other

All Publications (16 results)

  • [Publications] Hideaki Kawaguchi: "The studies of the cell damage and cell proliferation factors which induce cardiomyopathy." Jpn.Circ.J.56. 1037-1044 (1992)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Kazushi Urasawa: "The mechanism of cathecholamin-tolerance in heart failure:the change of Adenylyl cyclase system" Jpn.Circ.J.56. 456-461 (1992)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Mikako Shoki: "Phosphatidylinositol metabolism in hypertrophic rat heart" Jpn.Circ.J.56. 142-147 (1992)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Kenji Iizuka: "Effect of hypoxia on calcium activated neutral protease activity in myocytes." Jpn.Heart J.33. 707-715 (1992)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Hirofumi Sawa: "Expression of the angiotensinogen gene and localization of its protein in the human heart" Circulation. 86. 138-146 (1992)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Hideaki Kawaguchi: "Inositolphophatides metabolism in hypertrophic rat heart" J.Mol.Cell Cardiol.24. 1003-1010 (1992)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Hideaki Kawaguchi: "PI response and calcium overload in cardiomyopathic hamster heart cells.New Aspect in the Treatment of Failing Heart" Springer-Verlag, 5(36-40) (1992)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Kazushi Urasawa: "A mechanism of cathecholamin Tolerance in congestive heart failure New Aspect in the Treatment of Failing Heart" Springer-Verlag, 6(75-80) (1992)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] HIDEAKI KAWAGUCHI: "THE STUDIES OF THE CELL DAMAGE AND CELL PROLIFERATION FACTOR WHICH INDUCE CARDIOMYOPATHY" JPN CIRC J. 56. 1037-1044 (1992)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] KAZUSHI URASAWA: "THE MECHANISIM OF CATHECHOLAMIN-TOLERANC IN HEART FAILURE : THE CHANGE OF ADENYLYL CYCLASE SYSTEM" JPN CIRC J. 56. 456-461 (1992)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] "PHOSPHATIDYLINOSITOL BETABOLISM IN HYPERTROPHIC RAT HEART" JPN CIRC J. 56. 142-147 (1992)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] KENJI IIZUKA: "EFFECT OF HYPOXIA ON CALCIUM ACTIVATED NEUTRAL PROTEASE ACTIVITY IN MYOCYTES" JPN HEART J. 33. 707-715 (1992)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] HIROFUMI SAWA: "EXPRESSION OF THE ANGIOTENSINOGEN GENE AND LOCALIZATION OF ITS PROTEIN IN THE HUMAN HEART" CIRCULATION. 86. 138-146 (1992)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] HIDEAKI KAWAGUCHI: "INOSITOLPHOSPHATIDES METABOLISM INHYPERTROPHIC RAT HEART" J MOL CELL CARDIOL. 24. 1003-1010 (1992)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] HIDEAKI KAWAGUCHI: PI RESPONSE AND CALCIUM OVERLOAD IN CARDIOMYOPATHIC HAMSTER HEART CELLS.NEW ASPECT IN THE TREATMENT OF FAILING HEART EDD YASUDA AND KAWAGUCHI. SPRINGER-VERLAG, 36-40 (1992)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] KAZUSHI URASAWA: A MECHANISM OF CATHECHOLAMINE TOLERANCE IN CONGESTIVE HEART FAILURE.NEW ASPECT IN THE TREATMENT OF FAILING HEART EDD YASUDA AND KAWAGUCHI. SPRINGER-VERLAG, 75-80 (1992)

    • Description
      「研究成果報告書概要(欧文)」より

URL: 

Published: 1995-03-27  

Information User Guide FAQ News Terms of Use Attribution of KAKENHI

Powered by NII kakenhi