| Project/Area Number |
61570165
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Experimental pathology
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| Research Institution | Institute of Medical Science, University of Tokyo |
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Principal Investigator |
MATSUZAW akio Institute of Medical Science, University of Tokyo, 医科学研究所, 助教授 (50012745)
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| Co-Investigator(Kenkyū-buntansha) |
TANAKA Shin Institute of Medical Science, University of Tokyo, 医科学研究所, 教務職員 (70134624)
KIMURA Mikio Institute of Medical Science, University of Tokyo, 医科学研究所, 助手 (90114462)
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| Project Period (FY) |
1986 – 1987
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| Project Status |
Completed (Fiscal Year 1987)
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| Budget Amount *help |
¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 1987: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1986: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | Basement membrane / type IV collagen / mice / kidney / early development / hereditary cataract / lens / autoimmune disease / hormone-dependent mammary tumor / 進展 / 自律性獲得 / 転移 / 【IV】型コラーゲン / マウス腎臓 / マウス初期発生 / コンパクション |
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| Research Abstract |
Type IV collagen was isolated and purified from mouse kidneys and the antiserum against it was raised in rabbits. Immunofluorescence and immunohistochemical staining methods were established and applied to research into the roles of the collagen in early or preimplantation development of mice, cataractogenesis in hereditary cataract mice, pathological changes of the kidney in autoimmune mice and progression toward more malignant states of mouse mammary tumors. The specific inhibitor of collagen synthesis, cis-4-hydroxyproline, suppressed compaction of mouse embryos in culture in support of the important role of collagens in morphogenesis in early development. Participation of type IV collagen in this phenomenon is under observation by immunohistochemistry. No evidence has been obtained to indicate a significant role of type IV collagen in lens opacification in hereditary congenic catract mice, BALB/c-nct/nct. Graft-versus-host reaction and hereditary CBA/KI autoimmune mice were used as models for investigation of renal pathogenesis. Immunohistochemical studies with the antiserum against type IV collagen demonstrated that the basement membranes became thicker and more fragile along with pathological changes of the kidney in these models. This is in accord with the disturbed renal dysfunction documental by proteinuria. The amounts of extracellular matrices and type IV collagen, and the collagen-producing capability reduced with progression of hormone-dependent mouse mammary tumor, TPDMT-4, to autonomous and further to metastatic states, suggesting the significant role of collagens in tumor progression.
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