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2000 Fiscal Year Final Research Report Summary

Studies on the hormonal and immunological mechanisms for maintenance of mammalian uterine structure

Research Project

Project/Area Number 10304064
Research Category

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

Allocation TypeSingle-year Grants
Section一般
Research Field 生物形態・構造
Research InstitutionThe University of Tokyo

Principal Investigator

MORI Takuo  Graduate School of Science, The University of Tokyo, Professor, 大学院・理学系研究科, 教授 (80011659)

Co-Investigator(Kenkyū-buntansha) AKAGOME Yasuhisa  Graduate School of Science, The University of Tokyo, Instructor, 大学院・理学系研究科, 助手 (50302807)
MATSUDA Manabu  Graduate School of Science, The University of Tokyo, Instructor, 大学院・理学系研究科, 助手 (30282726)
Project Period (FY) 1998 – 2000
Keywordsuterus / morphology / collagen / metalloproteinase / stromal cell / muscle cell / invasion / mouse
Research Abstract

Mammalian uterus is an important reproductive organ for pregnancy. Although drastic structural changes occur in uterine tissues during the estrous cycle or pregnancy, the border between the endometrium and myometrium is always maintained in a constant state. In the uterus, there is no distinct barrier such as a basement membrane between the endometrium and myometrium. Invasion of the endometrial tissues into the musculature is blocked by a tight band of smooth muscle cells and extracellular matrix (ECM). However, hormonal imbalance can destroy the firm arrangement of the two tissues, resulting in the invasion of endometrial tissues into the musculature, a condition which is known as adenomyosis. The process of cell migration or invasion is associated with the degradation and reconstruction of the surrounding microenvironment consisting of ECM.Development of adenomyosis may be associated with the ECM-degrading ability of stromal cells and/or the degradation of the ECM in the muscle layer. It is well known that matrix metalloproteinases (MMPs) are important enzymes in the degradation and remodeling of the ECM, and may also play significant roles in cell movement. Stromal cells obtained from adenomyotic uteri markedly invaded the reconstituted basement membrane containing type IV collagen but not type I, III and V.MMP inhibitor suppressed the invasion. The stromal cells from normal uteri showed minimal invasion into gels consisting of collagen types I, III, or V.These data imply that ECM containing type I, III, and V collagen in the musculature is generally protective against the invasion of stromal cells.

  • Research Products

    (12 results)

All Other

All Publications (12 results)

  • [Publications] Mori,T.: "Animal model of uterine adenomyosis : Induction of the lesions in rats by ectopic pituitary isografting"Laboratary Animal Science, USA. 48. 64-68 (1998)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Sasabe,H.: "Histochemical analysis using lectin in the mouse uterine tissues with experimentally-induced adenomyosis"Acta Histochemistry and Cytochemistry. 31. 105-112 (1998)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Yamashita,M.: "In situ detection of prolactin receptor mRNA and apoptotic cell death in mouse uterine tissue with adenomyosis"In Vivo. 13. 57-60 (1999)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Zhou,Y-F.: "Effect of mifepriston treatment on the development of uterine adenomyosis induced by pituitary grafting"Life Science. 67. 2713-2720 (2000)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Matsuda,M.: "Increased invasion activity of endometrial stromal cells and elevated expreseion of MMP mRNA in the uterine tissues in mice."American Journal of Obstetrics and Gynecology. (印刷中). (2001)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Mori,T.: "Suppression of the development of uterine adenomyosis by a novel MMP inhibitor ONO-4817, in mice"Experimental Biology and Medicine.. (印刷中). (2001)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] T.Mori, M.Kyokuwa and H.Nagasawa: "Animal model of uterine adenomyosis : Induction of the lesion in rats by ectopic pituitary isografting."Lab.Anim.Sci.. 48. 64-68 (1998)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] H.Sasabe, M.Matsuda and T.Mori: "Histochemical analysis using lectin in the mouse uterine tissues with experimentally-induced adenomyosis."Acta Hisotchem.Cytochem.. 31. 105-112 (1998)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] M.Yamashita, M.Matsuda and T.Mori: "In situ detection of prolactin receptor mRNA and apoptotic cell death in mouse uterine tissues with adenomyosis."In Vivo. 13. 57-60 (1999)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] Y-F.Zhou, M.Matsuda, T.Mori, S.Sakamoto and T.Mitamura: "Effects of mifepristone (RU486) treatment on the development of uterine adenomyosis induced by pituitary grafting in mice."Life Sci.. 67. 2713-2720 (2000)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] M.Matsuda, H.Sasabe, Y.Adachi, T.Suzuki and T.Mori: "Increased invasion activity of endometrial stromal cells and elevated expression of matrix metalloproteinase mRNA in the uterine tissues of mice with experimentally induced adenomyosis."Am.J.Obset.Gynecol.. (in press).

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] T.Mori, S.Yamasaki, F.Masui, M.Matsuda, H.Sasabe and Y-F.Zhou: "Suppression of the development of experimentally induced uterine adenomyosis by a novel matrix metalloproteinase inhibitor, ONO-4817, in mice."Exp.Biol.Med.. (in press).

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

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Published: 2002-03-26  

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