| Project/Area Number |
06670889
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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 |
Dermatology
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| Research Institution | Chiba University (1995)
Kawasaki Medical School (1994) |
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Principal Investigator |
HATAMOCHI Atsushi Chiba University School of Medicene, lecturer, 医学部付属病院, 講師 (90172923)
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| Co-Investigator(Kenkyū-buntansha) |
KURODA Kei Chiba University School of Medicine, Assistant, 医学部, 助手 (90225300)
SHINKAI Hiroshi Chiba University School of Medicine, Professor, 医学部, 教授 (90030957)
長橋 美江 川崎医科大学, 医学部, 助手 (40258231)
愛甲 隆昭 川崎医科大学, 医学部, 助手 (30258230)
渡辺 圭介 川崎医科大学, 医学部, 助手 (80268606)
植木 宏明 川崎医科大学, 医学部, 教授 (30069017)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1995: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1994: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Keywords | type l collagen / fibrosis / transcription / TNF-alpha / type Vl collagen / collagenase / cutis laxa / TNF‐α / VI型コラーゲン / cutis laxa / 皮膚線維症 / α_1(I)コラーゲン / 遺伝子 / DNA結合因子 |
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| Research Abstract |
Although the expression of type I collagen in filbrotic skin diseases is known to be controlled at the transcriptional level, the control mechanism is poorly understood. We have investigated suppression mechanisms of the transcription of human alpha1 (1) collagen gene by tumor necrosis factor-alpha, and found that the transcription is suppressed through elements located between-101 and-97bp, and between-46 and-38bp of alpha1 (1) collagen gene promoter. We also investigated the regulation of type Vl collagen, and we have found that expression of type Vl collagen genes is increased in cutis laxa fiboblasts. Alterd activity of collagen degradation is another possible mechanism of excessive accumulation of collagen in fibrotic skin diseases. We have found that collagenase gene expression in cutis laxa filbroblasts is upregulated by transcriptional activation of the promoter gene through a TPA-responsive element.
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