Elucidation of the signaling mechanism of the novel stress mediator 12-HETE

2017 Fiscal Year Final Research Report

• Project/Area Number: 16K15197
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Environmental physiology(including physical medicine and nutritional physiology)
• Research Institution: National Institute of Advanced Industrial Science and Technology
• Principal Investigator: SHICHIRI Mototada 国立研究開発法人産業技術総合研究所, バイオメディカル研究部門, 研究グループ長 (20434780)
• Project Period (FY): 2016-04-01 – 2018-03-31
• Keywords: ストレス / 脂質酸化物 / 脳内モノアミン

Outline of Final Research Achievements

We had founded that 12-HETE, 12-lipoxygenase metabolite of arachidonic acid, specifically increased in mouse plasma after stress load. And, we also demonstrated that 12-HETE induces the escape behavior. However, 12-HETE did not increase in mouse brain tissue after stress load, the signal pathway by which 12-HETE increased in plasma transmits to the brain was unclear. In this study, we hypothesized that 12-HETE signal are transmitted to the brain via the 12-HETE receptor expressed in peripheral nerves. We found out that the inhibitor of 12-HETE receptor could suppress the escape behavior and 12-HETE is involved in stress-induced release of noradrenaline in brain tissue. These results suggested that 12-HETE is a novel stress pathway different from the already known pathway.

Free Research Field

酸化ストレス