2013 Fiscal Year Final Research Report
Effects of oxidative stress on wound healing and hypertrophic scar formation process
Project/Area Number |
24791930
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Plastic surgery
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Research Institution | Hyogo Medical University |
Principal Investigator |
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Research Collaborator |
KAWAI Kenichiro 兵庫医科大学, 医学部, 准教授 (80423177)
ISHISE Hisako 兵庫医科大学, 医学部, 病院助手 (30567194)
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Project Period (FY) |
2012-04-01 – 2014-03-31
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Keywords | 酸化ストレス / TRPCチャネル / 創傷治癒 |
Research Abstract |
In inflammatory condition, oxidative stress increases where Reactive Oxygen species (ROS) damages cell function. On the other hand, ROS production is strictly regulated in the normal metabolism of cells and plays important roles in cell signaling. TRP channels react to a variety of environmental stress. Especially, TRPC subfamilies react to oxidative stress. ROS keeps TRPC channels open and Ca influx occurs which results in the increased Ca concentration in cytoplasm. Ca is known to be an important second messenger of cell signaling and the increase of Ca in cytoplasm causes several reaction. In this study, TRPC3 and 5 overexpressing fibroblasts were generated and and the function of these channeles in oxidative stress were analyzed. Fibroblast Populated Collagen Lattice with TRPC3 showed increased contractile activity in oxidative stressed condition.
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