| Project/Area Number |
01480316
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
General surgery
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| Research Institution | Keio university |
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Principal Investigator |
FUJINO Toyomi Keio University School of Medicine, Dept. Plastic Surgery, Professor, 医学部, 教授 (20051279)
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| Co-Investigator(Kenkyū-buntansha) |
MINABE Toshiharu Keio University School of Medicine, Dept. Plastic Surgery, Instructor, 医学部, 助手 (50200077)
KOBAYASHI Masahiro Keio University School of Medicine, Dept. Plastic Surgery, Instructor, 医学部, 助手 (30195812)
SEGAWA Kaoru Keio University School of Medicine, Dept. Microbiology, Assistant Professor, 医学部, 講師 (30114523)
TAKANO Toshiya Keio University School of Medicine, Dept. Microbiology, Professor, 医学部, 教授 (60051364)
今西 宣晶 慶應義塾大学, 医学部, 助手 (00184820)
栗原 卓也 慶應義塾大学, 医学部, 助手 (90186510)
長谷川 時生 慶應義塾大学, 医学部・形成外科, 助手 (00180860)
福積 聡 慶應義塾大学, 医学部・形成外科, 助手 (90181289)
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| Project Period (FY) |
1989 – 1991
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| Project Status |
Completed (Fiscal Year 1991)
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| Budget Amount *help |
¥4,900,000 (Direct Cost: ¥4,900,000)
Fiscal Year 1991: ¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 1990: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 1989: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | Wound healing / Keloid / Collagen synthesis / TGF-beta / Collagenase gene / Immortalization / Collagen mRNA / Regulation of cell proliferation / 創傷治癒 / 過形成 / 細胞異常増殖 / コラ-ゲン / 血管新生 / ヒトニ倍体細胞 / トランスフォ-メ-ション / SV40 largeT抗原 / 細胞不死化 / 染色体異常 / 細胞増殖速度 / 分子生物学 / プロコラ-ゲンα1(I)mRNA |
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| Research Abstract |
Procollagen ccl, mRNA was specifically expressed at higher levels in the experimental wound tissue on rat dorsal skin five to seven days after the injury. TGF-beta induced the expression of procollagen alphal MRNA at similar levels in the fibroblasts cultured from normal human skin and keloidal tissues. The incorporation of ^<14>C-leucine was three to five more in human fresh keloidal slices than those of normal dermis, suggesting that the hyperproduction of collagen was regulated at a translational level in keloid. The serum of patients with systemic severe keloid strongly stimulated the growth of cultured skin fibroblasts compared with normal human and fetal calf sera. Both higher concentration of growth-stimulating factors and activation of collagen production at a translational level seemed to be involved in the pathogenesis of keloid. In the study on the immortalization of SV40-transformed human diploid fibroblasts as an in vitro modpl of the abnormal proliferation in keloidal skin fibroblasts, certain mutational events responsible for immortalization occurred in crisis and the expression of collagenase gene was specifically shut off after immortalization. The synthesis and degradation of collagen seemed to be intrinsically related with the growth regulation in fibroblasts. In experimental skin pedicle flaps, we detected the prominent dilatation of small anastomotic arteries which seemed to play major roles in supplying blood cells releasing wound-healing factors rather than angiogenesis.
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