| Co-Investigator(Kenkyū-buntansha) |
佐々木 健 浜松医科大学, 大学院医学系研究科, 技術専門職員 (20397433)
菊地 良介 名古屋大学, 医学部附属病院, 臨床検査技師 (30721435)
坂東 泰子 (暮石泰子) 名古屋大学, 医学部附属病院, 講師 (60452190)
竹下 享典 名古屋大学, 医学部附属病院, 准教授 (70444403)
|
|---|
| Budget Amount *help |
¥17,810,000 (Direct Cost: ¥13,700,000、Indirect Cost: ¥4,110,000)
Fiscal Year 2017: ¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2015: ¥7,670,000 (Direct Cost: ¥5,900,000、Indirect Cost: ¥1,770,000)
|
|---|
| Outline of Final Research Achievements |
Exposure to psychosocial stress is a risk factor for cardiovascular disease. Here, we have used dipeptidyl peptidase-4 (DPP4)-deficient mice and its inhibitor as well as glucagon-like peptide-1 (GLP-1) receptor agonist to explore the role of DPP4/GLP-1 axis in ischemia-induced neovascularization and diet-induced atherosclerosis. We demonstrated that stress impaired the recovery of the ischemic/normal blood-flow ratio throughout the follow-up period and capillary formation; and these changes DPP4 inhibition and GLP-1R activation improved these changes; these benefits were abrogated by adiponectin blocking and genetic depletion. Similarly, chronic stress accelerated diet-induced atherosclerotic lesion formation; and this effect was reversed by DPP4 inhibition. Our findings suggest that CatK might be a new therapeutic target for the chronic psychological stress-related neovascularization and cardiovascular diseases.
|
