2001 Fiscal Year Final Research Report Summary
Genomic Study on Keloids and Hypertrophic Scars
| Project/Area Number |
12671753
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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 |
HYAKUSOKU Hiko Nippon Medical School, Medical Science, Professor, 医学部, 教授 (00165135)
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| Co-Investigator(Kenkyū-buntansha) |
NAKAZAWA Nando Nippon Medical School, Medical Science, Lecturer, 医学部, 講師 (20010051)
MURAKAMI Masahiro Nippon Medical School, Medical Science, Instructor, 医学部, 助手 (00239500)
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| Project Period (FY) |
2000 – 2001
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| Keywords | KELOID / HYPERTROPHIC SCAR / DNA-MICROARRAY / TUMOR SUPPRESSORS / SNP / PATHOLOGICAL GENOMICS / 細胞増殖 / Pathological Genomics |
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| Research Abstract |
We have studied and are continuing to study the cellular 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.
The results are as follows ;
1) The tissue LDH levels assayed using a 1H-NMR technic were found to be closely associated with diagnostic and pathological gradings of the disease : a 1H-NMR assay of the tissue LDH levels provides effective conclusive diagnostic criteria for the disease.
2) Distribution of SNP of tumor suppressor gene, p53, at codon-72 region among keloid and hypertrophic scar patients was analyzed using RFLP method. It was indicated that Arginine-encoding sequence (CGC) and Proline-encoding sequence (CCC) confer genetic predisposition to earlobe keloids and hypertrophic scars, respectively.
3) To investiga
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te the function of P53 proteins with different amino - acid at codon-72 region, cells which express either Arg-P53 or Pro-P53 protein were grown in the various culture conditions. Arg-P53 cells were found to be more sensitive to high temperature conditions than Pro-P53 cells.
4) The pathological genomics of keloids was performed using the cDNA microarray technic after extracting mRNA from keloid fibroblastic cells in culture. Eight genes and 17 genes were expressed specificly from earlobe keloid cells and chest keroid cells, respectively. Thrombin receptor gene, KIAA0367 protein gene and matrilin-2 gene were typical genes expressed specifically in both of the keloid fibroblastic cells. Screening for the gene that is known to be involved in the growth regulating mechanism of cells revealed that a tumor suppressor gene is expressed only in the normal control skin fibroblasts but not in keloid cells. The result implies that the growth suppressor gene is implicated in the pathogenesis of keloid lesion. Less
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