Development of pharmacotherapy which targets TGF beta /Smad signal for skin scarring.

• Project/Area Number: 25462829
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Emergency medicine
• Research Institution: Wakayama Medical University
• Principal Investigator: MAKI KIDA 和歌山県立医科大学, 医学部, 講師 (00326381)
• Co-Investigator(Kenkyū-buntansha): Ueda Kentaro 和歌山県立医科大学, 医学部, 講師 (20438279)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Project Status: Completed (Fiscal Year 2015)
• Budget Amount: ¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000); Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000); Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000); Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
• Keywords: 瘢痕 / 創傷治癒 / TGFβ / オステオポンチン / Smad / オステオポンチン中和抗体 / 皮膚創傷治癒 / 皮膚の創傷治癒 / TGFｂ / TGFベータ / 皮膚

Outline of Final Research Achievements

For development of scarring skin wound pharmacotherapy of which a target is TGF β / Smad signals, we studied skin wound healin osteopontin (OPN) knockout mice.
The wound healing of skin delayed, formation of granuration and TGFb signal were inhibited in OPN mice.OPN neutralizing antibody inhibited expressions of fibronectin,collagen Ia1,aSMA in wild type (WT) mice.OPN neutralizing antibody suppresed the formation of the granulation tissue and may inhibit scarring in skin wound.

Research Products

• [Presentation] Lacking osteopontin impairs TGFβ/Smad signal and attenuates healing of a full-thickness cutaneous wound in mice (2016)
  • Author(s): 木田 真紀
  • Organizer: Keystone Symposia
  • Place of Presentation: Keystone, US
  • Year and Date: 2016-02-09
  • Int'l Joint Research