Project/Area Number |
26860182
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Multi-year Fund |
Research Field |
General medical chemistry
|
Research Institution | Akita University |
Principal Investigator |
YASUDA DAISUKE 秋田大学, 医学(系)研究科(研究院), 助教 (70594951)
|
Project Period (FY) |
2014-04-01 – 2016-03-31
|
Project Status |
Completed (Fiscal Year 2015)
|
Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2015: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
Fiscal Year 2014: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
|
Keywords | Gタンパク質共役型受容体 / リゾホスファチジン酸 / 血管形成 / 血管形成異常 / 胎生致死 |
Outline of Final Research Achievements |
To reveal novel roles of LPA4 and LPA6 in embryonic blood vessel formation, LPA4-deficient mice were crossed with LPA6-deficient mice to generate the double mutants. Mouse embryos at different developmental stages were macroscopically observed. At embryonic day (E) 9.5-10.5, almost all of the LPA4/LPA6-double deficient mice had some morphological abnormalities, such as severe pericardial effusion, developmental delay, poor vascular network in head and intersomitic regions and enlarged dorsal aorta. Furthermore, the yolk sacs of LPA4/LPA6-double deficient lacked large vessels.. Of note, all double mutants died by E11.5.
|