Study on control of scar formation after cleft palate with a wound healing model using rat skin

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K11358
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Orthodontics/Pediatric dentistry
• Research Institution: Fukuoka Dental College
• Principal Investigator: Ishikawa Hiroyuki 福岡歯科大学, 口腔歯学部, 常務理事 (20184492)
• Co-Investigator(Kenkyū-buntansha): 沢 禎彦 岡山大学, 医歯薬学総合研究科, 教授 (70271666) ; 山崎 純 福岡歯科大学, 口腔歯学部, 教授 (50230397) ; 梶井 貴史 福岡歯科大学, 口腔歯学部, 准教授 (60322822) ; 中島 一記 福岡歯科大学, 口腔歯学部, 助教 (80610980) ; 秦 省三郎 福岡歯科大学, 口腔歯学部, 助教 (40736732)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: ケラチノサイト / 線維芽細胞 / TGF-β１ / TRPV2

Outline of Final Research Achievements

Postoperative scar tissue on palates is considered to induce maxillary growth inhibition in cleft lip and palate patients. We characterized the role of TRP channels in the release of TGF-β1 from keratinocytes and the differentiation of fibroblasts to identify possible promising pharmacological approaches to prevent scar formation and contractures. The 3D culture model was made from rat skin seeded on a collagen gel in which dermal fibroblasts had been embedded. Among the TRP channel inhibitors tested, the TRPV2 inhibitors attenuated most potently keratinocyte-dependent and -independent collagen gel contraction due to TGF-β signaling as well as TGF-β1 release from keratinocytes and α-SMA production in myofibroblasts. TRPV2 was expressed in the epidermis and keratinocyte layers of the model. Compounds targeting TRPV2 channels would ameliorate wound contraction through the inhibition of TGF-β1 release and the differentiation of dermal fibroblasts in a culture model.

Free Research Field

歯科矯正学