| Project/Area Number |
13671886
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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 |
Plastic surgery
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| Research Institution | Nippon Medical School |
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Principal Investigator |
GHAZIZADEH Mohammad Nippon Medical School Institute of Gerontology, Department of Molecular Pathology, Associate Professor, 老人病研究所, 助教授 (30190979)
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| Co-Investigator(Kenkyū-buntansha) |
KAWAKNAMI Oichi Nippon Medical School Institute of Gerontology, Department of Molecular Pathology, Professor, 老人病研究所, 教授 (70096973)
TOSA Mamiko Nippon Medical School, Department of Plastic and Reconstructive Surgery, Assistant Professor, 医学部, 助手 (30301568)
HIRAI Takashi Nippon Medical School, Department of Plastic and Reconstructive Surgery, Associate Professor, 医学部, 助教授 (40208799)
EMI Mitsuro Nippon Medical School Institute of Gerontology, Department of Molecular Biology, Professor, 老人病研究所, 教授 (90221118)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 2002: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2001: ¥900,000 (Direct Cost: ¥900,000)
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| Keywords | keloid / cDNA microarray / fibroblasts / gene expression / 繊維芽細胞 |
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| Research Abstract |
Keloid formation results from abnormal wound healing, however the molecular mechanisms regulating this process remain undetermined. With the advent of cDNA microarray technology, variations in cellular transcriptional events can be monitored simultaneously, and expression profile of each state can be established and compared to its counterpart state. We performed gene expression profile analysis of fibroblasts from healthy skin and keloid tissues after obtaining informed consents. Fibroblast cultures were established by outgrowth from healthy skin and keloid tissue samples obtained at surgery. After two subculturing, monolayer cells at 80-90% confluency were lysed, total RNA was extracted and ^<33>P-labeled cDNA probe was prepared. The probes were hybridized to Derm Array GeneFilters and the scanned filter images were analyzed and compared using the Pathways software. Several genes related to the cell cycling, apoptotsis, extracellular matrix formation/degradation, growth factors, protease inhibitors, and focal adhesions were identified. Among these, c-Abl (a tyrosine kinase) and cdc25A (a tyrosine phosphatase) were noteworthy because of their important roles in signal transduction pathways. We intend to further pinpoint the roles of these genes in the development of keloid using RNA interference (RNAi) method. Hitherto, our results suggest a "synthetic" fibroblast phenotype in keloid lesion chracterized by an accelerated cell cycle combined with induction of matrix synthesis and inhibition of matrix degradation. Identification of these genes that are involved in keloid formation may help better understand its molecular and cellular biology.
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