The relationship between the mechanical force and the interaction of skin-immune system during wound healing process

2017 Fiscal Year Final Research Report

• Project/Area Number: 16K15755
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Plastic surgery
• Research Institution: Hyogo Medical University
• Principal Investigator: Kawai Kenichiro 兵庫医科大学, 医学部, 准教授 (80423177)
• Co-Investigator(Kenkyū-buntansha): 藤原 敏宏 兵庫医科大学, 医学部, 非常勤講師 (00423179) ; 西本 聡 兵庫医科大学, 医学部, 教授 (30281124) ; 石瀬 久子 兵庫医科大学, 医学部, その他(移行) (30567194) ; 曽束 洋平 兵庫医科大学, 医学部, 講師 (40437413) ; 藤田 和敏 兵庫医科大学, 医学部, その他 (40461066) ; 垣淵 正男 兵庫医科大学, 医学部, 教授 (50252664)
• Project Period (FY): 2016-04-01 – 2018-03-31
• Keywords: 機械的伸展刺激 / 肥厚性瘢痕 / TRPC3 / EDNRB

Outline of Final Research Achievements

Hypertrophic Scar is a condition where high accumulation of collagen can be seen which is promoted by the excessive wound healing process. Main factors causing hypertrophic scar are (1). stretching force of wound site and (2). inflammation of wound. Although we tried to investigate the interaction between fibroblasts and dendritic cells under stretched condition, the research did not work well. However, meanwhile, we found the interaction between keratinocyte and fibroblasts under cyclic stretched condition. It is known that keratinocytes secret Endothelin-1 in response to the stretching force. In our study, cyclic stretching force is found to enhance the expression of Endothelin Receptor B and its coupling ion channel; TRPC3 and the sensitivity to Endothelin -1 signaling is increased. These findings suggest that the interaction between fibroblasts and keratinocytes during the wound healing process contribute to the formation of hypertrophic scar.

Free Research Field

形成外科