Intracellular signal transduction in response to hypothermia

2017 Fiscal Year Final Research Report

• Project/Area Number: 26670782
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Emergency medicine
• Research Institution: Yamagata University
• Principal Investigator: Goto Kaoru 山形大学, 医学部, 教授 (30234975)
• Co-Investigator(Kenkyū-buntansha): 秋元 亮 山形大学, 医学部, 助教 (40594677)
• Project Period (FY): 2014-04-01 – 2018-03-31
• Keywords: エネルギー代謝 / 脂質代謝酵素 / 低酸素 / エネルギーセンサー / ATP / 熱ショックタンパク質

Outline of Final Research Achievements

Upon tissue damage, hypothermia induces Hypoxia inducible factor (HIF), which suppresses energy expenditure and exerts a beneficial effect to damaged cells. In this study we examined the regulatory mechanism of the diacylglycerol kinase (DGK) family on HIF expression and energy metabolism. We found that after 24 h of 1% hypoxic conditions DGKzeta deficiency reduces HIF1alpha expression by 50%, activates energy sensor AMPK, and increases intracellular ATP levels. These results suggest that DGKzeta plays an important role in energy metabolism under hypoxic conditions.

Free Research Field

解剖学、組織学、細胞生物学