| Project/Area Number |
14370574
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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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 |
HYAKUSOKU Hiko Nippon Medical School, Medical Science, Professor, 大学院医学研究科, 教授 (00165135)
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| Co-Investigator(Kenkyū-buntansha) |
MURAKAMI Masahiro Nippon Medical School, Medical Science, Lecturer, 医学部, 講師 (00239500)
NAKAZAWA Nando Nippon Medical School, Medical Science, Lecturer, 医学部, 講師 (20010051)
石丸 さやか 日本医科大学, 医学部, 助手 (00297889)
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| Project Period (FY) |
2002 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥11,300,000 (Direct Cost: ¥11,300,000)
Fiscal Year 2004: ¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 2003: ¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2002: ¥6,200,000 (Direct Cost: ¥6,200,000)
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| Keywords | KELOIDS / HYPERTROPHIC SCARS / DNA-MICROARRAY / REAL-TIME PCR / PROTEOGALYCANS / EXTRACELLULAR MATRIX / ケロイド培養線維芽細胞 / lumican / decorin / microarray解析 / collagen形成 / promoter領域 / ケロイド / Real-Time PCR / c-erb B / Par-1 / Mda-7 / TGF-β1 / Decorin / 肥厚性瘢痕 / 細胞増殖 / マイクロビーズ・アレイ / II-24 / PAR-1 |
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| Research Abstract |
We have studied and are continuing to scrutinize the cellualr and molecular mechanism of pathogenesis of keloids and hypertrophic scars to develop the effective therapeutic procedure for the scar-forming diseases. The scope of this research is also directed further to elaborate clinical diagnostic and prognostic methods, and eventually to perform scar-free surgical operations.
1)Screening by using a cDNA-microarray method with 1000-probes for the gene that is known to be involved in the cell growth regulating mechanism revealed that a tumor suppressor gene, Mda-7,is expressed only in the normal control skin fibroblasts but not in keloid cells. The same cDNA-microarray showed that the expression of the thrombin receptor gene Par-1,a growth promoting factor receptor gene, is enhanced in the keloid fibroblastic cell lines. The result seemed to imply that the growth suppressor/promoter genes is implicated in the pathogenesis of keloid lesion.
2)Investigation of the growth characteristics of the keloid fibroblastic cells by succesive subcultures by the 1:2-splitting procedure indicated that the cellular life span of the keloid fibroblastic cells was not different from that of the normal diploid fibroblasts.
3)Although differences in the gene expression of decorin and lumican of keloid fibroblastic cells by using an oligoDNA-microarray method were detected, no significant differences in the expression of the genes were indicated between normal- and keloid-fibroblastic cells by Real-time PCR procedure.
4)The independent oligoDNA-microarray assay with 20,000 probes of 5 lines of the keloid fibroblastic cells that were derived from 5 individuals with the hereditary disposition to keloids against the mixed population of 3 normal skin fibroblastic cell lines as the control revealed the keloid fibroblast specific expression of 47 genes.
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