Analysis of regulation mechanisms of thermosensitive TRP channels and their involvement in immune responses

2014 Fiscal Year Final Research Report

• Project/Area Number: 23249012
• Research Category: Grant-in-Aid for Scientific Research (A)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: General physiology
• Research Institution: Okazaki Research Facilities, National Institutes of Natural Sciences
• Principal Investigator: TOMINAGA Makoto 大学共同利用機関法人自然科学研究機構(岡崎共通研究施設), 岡崎統合バイオサイエンスセンター, 教授 (90260041)
• Project Period (FY): 2011-04-01 – 2015-03-31
• Keywords: 生理学 / 神経科学

Outline of Final Research Achievements

Thermosensitive TRPM2 channels expressed in mouse mucosal mast cells were found to participate in antigen-induced extracellular Ca2+ influx and subsequent degranulation. In addition, hydrogen peroxide was found to lower the temperature threshold for TRPM2 activation through methionine oxidation, indicating that temperature threshold for TRPM2 activation is regulated by redox signals that enable channel activity at physiological body temperatures. Loss of TRPM2 attenuated zymosan-evoked macrophage functions, including cytokine release and fever-enhanced phagocytic activity. The hydrogen peroxide-induced TRPM2-sensitization mechanism through oxidation was also found to work in mouse pancreatic  cells where glucose-induced oscillation of intracellular Ca2+ concentrations and insulin release was TRPM2- and redox status-dependent.

Free Research Field

分子細胞生理学