Role of N-acetyl-glucosamine Metabolism in the Regulation of Macrophage Function and Atherosclerosis

2014 Fiscal Year Final Research Report

• Project/Area Number: 24591117
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Circulatory organs internal medicine
• Research Institution: Kyushu University
• Principal Investigator: KITAMOTO Shiro 九州大学, 医学(系)研究科(研究院), 講師 (00380436)
• Research Collaborator: BOISVERT William A. ; SUNAGAWA Kenji ; ICHIKI Toshihiro
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: 動脈硬化 / マクロファージ / シグナル伝達 / 生体分子 / 糖鎖

Outline of Final Research Achievements

O-linked N-acetyl-glucosamine (O-GlcNAc) modification was suggested to have anti-inflammatory effects of reducing M1 phenotype activation via inhibition of NF-κB transcriptional activity in cultured macrophages (Mφ), whereas augmentation of O-GlcNAc modification had no significant effects on atherosclerotic lesions of apoE deficient mice fed with Western diet. Because this apoE deficient mouse model shows hyperlipidemia and hyperglycemia and the anti-inflammatory effects of O-GlcNAc modification were blunted in high-glucose condition in cultured macrophages, O-GlcNAc modification is suggested to complexly regulate macrophage functions and mediate both anti-inflammatory and pro-inflammatory effects in the pathogenesis of atherosclerosis.

Free Research Field

医歯薬学