2006 Fiscal Year Final Research Report Summary
Investigation of keloid derived "stem-like" cells to clarify keloid pathogenesis.
| Project/Area Number |
17591874
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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 | Kyoto University |
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Principal Investigator |
NAITOH Motoko Kyoto Univ., Grad. School of Med., Dept. of Plast. & Reconstr. Surgery., Lecturer, 医学研究科, 助手 (30378723)
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| Co-Investigator(Kenkyū-buntansha) |
UTANI Atsushi Kyoto Univ., Grad. School of Med., Dept. of Dermatology., Assoc. Prof., 医学研究科, 助教授 (10292707)
NAGATA Kazuhiro Kyoto Univ., Institute for Frontier Medical Science, Dept. of Molecular and Cellular Biology., Prof., 再生医科学研究所, 教授 (50127114)
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| Project Period (FY) |
2005 – 2006
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| Keywords | Keloid / Wound Healing / Stem Cell / Reprogramming |
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| Research Abstract |
Keloids are a dermal fibrotic disease whose etiology remains unknown and for which there is no successful treatment. Here, we employed cDNA microarray analysis to examine gene expression in keloid lesions and control skin tissue. We found that 32 genes among the 9,000 tested were strongly up-regulated in keloid lesions, of which 21 were confirmed by Northern blotting. These included at least 7 chondrocyte/osteoblast marker genes, and RT-PCR analysis revealed that transcription factors specific for these genes, SOX9 and CBFA1, were induced. Immunostaining and in situ hybridization further supported that these markers are expressed in keloid lesions. Intriguingly, scleraxis, a transcription factor known as a marker of tendons and ligaments, was also induced in keloid fibloblasts. These gene expression patterns closely resemble to profiles of stem cells in tendon/ligament. Furthermore, we succeeded culture of "stem-like" cells derived from keloids, using the base medium according to Toma (Nat. Cell. Biol. 3:778-784, 2001) with supplement A. We propose that reprogramming of gene expression or disordered differentiation in skin-progenitor cells, from a dermal pattern to that of a chondrocytic/osteogenic lineage, probably closer to that of tendon/ligament lineage, may be involved in the etiology of keloids.
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