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Effects of oxidative stress on wound healing and hypertrophic scar formation process

Research Project

Project/Area Number 24791930
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Plastic surgery
Research InstitutionHyogo Medical University

Principal Investigator

FUJITA Kazutoshi  兵庫医科大学, 医学部, 助教 (40461066)

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)
Project Period (FY) 2012-04-01 – 2014-03-31
Project Status Completed (Fiscal Year 2013)
Budget Amount *help
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2012: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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.

Report

(3 results)
  • 2013 Annual Research Report   Final Research Report ( PDF )
  • 2012 Research-status Report

URL: 

Published: 2013-05-31   Modified: 2019-07-29  

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