Endothelial dysfunction after lung transplantation with donation after cardiac death donors

• Project/Area Number: 26462128
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Respiratory surgery
• Research Institution: Ehime University
• Principal Investigator: Okazaki Mikio 愛媛大学, 医学部附属病院, 助教 (50467750)
• Co-Investigator(Kenkyū-buntansha): 佐野 由文 愛媛大学, 医学系研究科, 准教授 (60322228)
• Project Period (FY): 2014-04-01 – 2018-03-31
• Project Status: Completed (Fiscal Year 2017)
• Budget Amount: ¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000); Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000); Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000); Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
• Keywords: 肺移植 / 虚血再灌流障害 / 心停止ドナー

Outline of Final Research Achievements

The purpose of this study was to elucidate molecular mechanism of ischemia reperfusion injury after lung transplantation with donation after cardiac death donors and to reduce lung transplantation with donation after cardiac death donors by using mouse model. Endothelial cells of donor lung were destroyed during ischemia period, and the inhibition of endothelial dysfunction is thought to be important on the reduction of ischemia reperfusion injury. R-spondin 3 which has been reported to tighten of endothelial cell junctions reduced lung warm ischemia reperfusion injury. Tightening of endothelial cell junctions was considered to contribute on the inhibition of lung warm ischemia reperfusion injury.