Development of membrane protein function analysis and the new suppression mediated by the tumor necrosis factor precursor and producing enzyme

2014 Fiscal Year Final Research Report

• Project/Area Number: 24590949
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Gastroenterology
• Research Institution: Nagoya City University
• Principal Investigator: JOH Takashi 名古屋市立大学, 医学(系)研究科(研究院), 教授 (30231369)
• Co-Investigator(Kenkyū-buntansha): TANIDA Satoshi 名古屋市立大学, 大学院医学研究科, 講師 (30528782)
• Co-Investigator(Renkei-kenkyūsha): HIGASHIYAMA Shigeki 愛媛大学, 大学院医学系研究科, 教授 (60202272)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: ADAM17 / ARP36-2 / TNFα / 新規治療ターゲット / 炎症性腸疾患

Outline of Final Research Achievements

Colon epithelial cells, many expressed in monocyte cells I was paying attention to the ARP 36-2 seen. When IL-1β stimulates colon epithelial cell line, TNFα concentration in the culture solution in over time increased but TPA, LPS, increase was observed. On the other hand, when the monocytic cell line TPA stimulation, TNFα concentration in the culture solution is increased, IL-1β, the stimulation with TPA, increase was observed. Further, when the deletion of the ADAM17 by KB-R7785, siRNA, colon epithelial cells, IL-1β in the monocyte cell, the concentration increase due to TPA stimulation during TNFαshedding, was significantly inhibited. Furthermore, even if lacking the ARP36-2 by siRNA, similarly concentration rise due to IL-1β, TPA stimulus during TNFαshedding has been significantly suppressed. ARP36, it seemed to be made in inflammatory bowel disease novel therapeutic target to control the TNFαshedding.

Free Research Field

消化器内科学