Analysis of wound healing mechanism in novel metabolic syndrome model mice

• Project/Area Number: 24592706
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Plastic surgery
• Research Institution: University of Tsukuba
• Principal Investigator: SASAKI Kaoru 筑波大学, 医学医療系, 講師 (10536220)
• Co-Investigator(Kenkyū-buntansha): WARABI Eiji 筑波大学, 医学医療系, 講師 (70396612) ; YANAGAWA Toru 筑波大学, 医学医療系, 准教授 (10312852)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Project Status: Completed (Fiscal Year 2014)
• Budget Amount: ¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000); Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000); Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000); Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
• Keywords: 創傷治癒 / 紫外線 / アポトーシス / A170 / UVA / 酸化ストレス / メタボリックシンドローム

Outline of Final Research Achievements

p62 gene knockout mice exhibit obesity and metabolic syndrome due to hyperphagia. In this study, we analyzed sensitivity to ultraviolet irradiation induced apoptosis using p62-KO mice and primary cells isolated from mice. As a result, we found deletion of p62 cause apoptosis resistance in both in vitro and in vivo level. The enhancement of transcription factor Stat3 activity seems to be involved in this phenotype by inducing anti-apoptotic protein induction. These results suggest that p62 is a novel factor to regulate Stat3 activity.