2004 Fiscal Year Final Research Report Summary
| Project/Area Number |
15591168
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Dermatology
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| Research Institution | Chiba University |
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Principal Investigator |
SHINKAI Hiroshi Chiba University, Graduate School of Medicine, Dermatology, Professor, 大学院・医学研究院, 教授 (90030957)
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| Co-Investigator(Kenkyū-buntansha) |
UTANI Atsushi Chiba University, Graduate School of Medicine, Dermatology, Assistant professor, 大学院・医学研究院, 助教授 (10292707)
ENDO Hideharuo Chiba University, Graduate School of Medicine, Dermatology, Assistant, 大学院・医学研究院, 助手 (50282489)
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| Project Period (FY) |
2003 – 2004
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| Keywords | collagen / proteoglycans / decorin / dermatopontin / fibrillogenesis |
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| Research Abstract |
Procollagen type I gene more increased in fibroblasts from patient with systemic sclerosis than fibroblasts from normal human skin, but gene expressions of decorin, thrombospondin, fibromodulin, type V and type XVI collagen were no different from normal human skin fibroblasts. P 38 MAPK was phosphorated by cytokines of TGF-β, PDGF and IL4 and these cytokines activate the gene exprssion of procollagen type I. The inhibitor of p38 MAPK decreased the expression of type I collage gene and increased interstitial collagenases.
We found the dermatopontin is a causative gene of Ehlers-Danlos syndrome. Gene expressions of dermatopontin showed an increased tendency to form granulation tissues with enhanced during 3 weeks in the case of process of wound healing. Whereas dermatopntin decreased in fibroblasts from hypertrophic scar and systemic sclerosis, the gene expressions of thrombospondin, fibromodulin and collage type XVI showed not alterd compared with normal human fibroblasts. IL-4 affects the decreasing gene expression of dermatopontin from fibroblasts of systemic sclerosis, and these cells increased the Il-4 receptor. There is evidence that the extracellular matrix protein dermatopontin may be important in the processe of remodeling in fibrillogenesis.
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