2018 Fiscal Year Final Research Report
Experiment of autophagy in keloidal collagen
| Project/Area Number |
17K17023
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Plastic surgery
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| Research Institution | Fukushima Medical University |
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Principal Investigator |
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| Research Collaborator |
Waguri Satoshi
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| Project Period (FY) |
2017-04-01 – 2019-03-31
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| Keywords | ケロイド / オートファジー / LC3 / Atg16L / ｂFGF / TGF-b |
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| Outline of Final Research Achievements |
The autophagy refers to a phenomenon to break down a cell ingredient of the self into in lysosome. It was reported recently that an autophagy-lysosomal system was affected in a fibroblast of the granulation tissues of the rat wound healing model. The condition of a patient caused by the fibroblastic abnormality increase includes a keloid. I used NRK cell derived from a rat fibroblast for the purpose of investigating sounding out and a cell growth factor, participation in autophagy of the differentiation factor thoroughly, and the researcher analyzed a cause of the increase of the number of the LC3-positive granules in the mammalian fibroblast about an effect of bFGF and transforming growth factor-beta in consideration of the possibility that abnormality of autophagy in the fibroblast caused a keloid.
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| Free Research Field |
形成外科
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| Academic Significance and Societal Importance of the Research Achievements |
bFGF投与によりLC3陽性顆粒数は増加せず、オートファジーによる分解も変化しなかった。TGF-β投与によりLC3陽性顆粒数は変化せず、オートファジーによる分解も変化しなかった。bFGF投与により隔離膜マーカーであるAtg16Lが増加するが、TGF-β投与72時間によりAtg16Lは減少した。以上より現時点で、bFGFやTGF-βがオートファジー分解系のどの段階に影響を与えているかを示すことができなかった。これは、LC3ないしAtg16L以外の抗体を使用して、オートファジー分解系の初期あるいは後期段階での動向の調査が必要であると考える。
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