Investigation concerning the pathogenesis of septic condition, and development of new therapy by PPARγ activation in monocytic cells.

Research Project

Project/Area Number	23792079
Research Category	Grant-in-Aid for Young Scientists (B)
Allocation Type	Multi-year Fund
Research Field	Emergency medicine
Research Institution	Kyoto Prefectural University of Medicine
Principal Investigator	FUKAZAWA Madoka 京都府立医科大学, 医学部附属病院, 専攻医 (30530357)
Project Period (FY)	2011 – 2012
Project Status	Completed (Fiscal Year 2012)
Budget Amount *help	¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000) Fiscal Year 2012: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000) Fiscal Year 2011: ¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
Keywords	遺伝子治療 / 敗血症 / RNA干渉法 / 単球系細胞
Research Abstract	We obtained macrophage from healthy volunteers. After the differentiation into macrophage, they were cultured in different glucose concentrations of cell culture liquid for 72 hours after lipopolysaccharide administration. High glucose conditions reduced phagocytic ability and exaggerated cell death in macrophage by the activation of endoplasmic reticulum stress. Ghrelin administration reversed these effects through peroxisome proliferator-activated receptor (PPARγ) activation.