Pathology and molecular mechanism of embryonic edema in mice carrying endothelial gene mutations
Project/Area Number |
22590173
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
General anatomy (including Histology/Embryology)
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Research Institution | Kobe University |
Principal Investigator |
|
Co-Investigator(Renkei-kenkyūsha) |
MORIWAKI Kazumasa 神戸大学, 大学院・医学研究科, グローバルCOE 研究員 (00467656)
DING Guo 神戸大学, 大学院・医学研究科, グローバルCOE 研究員 (00514697)
|
Project Period (FY) |
2010 – 2012
|
Project Status |
Completed (Fiscal Year 2012)
|
Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2010: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
|
Keywords | 発生学 / 形態形成学 / マウス / 遺伝子変異 / 発生 / 胎生期浮腫 / リンパ管 / 血管 |
Research Abstract |
We analyzed vascular permeability and development of the heart, blood vessels, and lymphatic vessels in Aspp1-/- and Flt1+/- mice showing embryonic edema. Lymphatic vascular development is defective in Aspp1-/- embryos, whereas vascular permeability is enhanced in Flt1+/- embryos with enhancement ofFlk1 phosphorylation. Transmission electron microscopic analysis reveals an intricateluminal surface and huge vesicle-like structures in Flt1+/- capillary endothelial cells,suggesting a promoted transcellular transport. Our analysis also shows that defectivelymphatic vessels and enhanced vascular permeability cause embryonic lethality of Aspp1-/-;Flt1+/- mice.
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Report
(4 results)
Research Products
(13 results)