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2016 Fiscal Year Final Research Report

Functional roles of arginine methylation on vascular networks for nutritional supply

Research Project

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Project/Area Number 25252062
Research Category

Grant-in-Aid for Scientific Research (A)

Allocation TypeSingle-year Grants
Section一般
Research Field Applied molecular and cellular biology
Research InstitutionUniversity of Tsukuba

Principal Investigator

FUKAMIZU Akiyoshi  筑波大学, 生命領域学際研究センター, 教授 (60199172)

Co-Investigator(Renkei-kenkyūsha) ISHIDA Junji  筑波大学, 生命領域学際研究センター, 講師 (30323257)
KAKO Koichiro  筑波大学, 生命環境系, 講師 (60311594)
KIM Jun-Dal  筑波大学, 生命領域学際研究センター, 講師 (90570036)
SUGIYAMA Fumihiro  筑波大学, 医学医療系, 教授 (90226481)
KASUYA Yoshitoshi  千葉大学, 医学系研究科, 准教授 (70221877)
Project Period (FY) 2013-04-01 – 2017-03-31
Keywords栄養 / 血管 / PRMT1 / 内皮細胞特異的ノックアウトマウス / イメージング / 透明化 / 二光子顕微鏡 / 代謝
Outline of Final Research Achievements

Angiogenesis is important in embryonic development, and endothelial cells play a critical role in these processes. Protein arginine methyltransferase 1 (PRMT1) is involved in multiple cellular functions including proliferation and differentiation, and is expressed in vascular endothelial cells, which are responsible for angiogenesis during embryonic development. Since homozygous mutation of the Prmt1 gene results in early embryonic lethality in mice, little has been known about its physiological importance. In the present study, we found that the endothelial cell-specific PRMT1 deficient mice (PRMT1-ECKO) died within embryonic day 15. Macroscopic observation showed that the temporal arteries were poorly perfused with blood as compared with controls. Whole mount in vivo 3D imaging revealed the dilated and segmentalized luminal structures in PRMT1-ECKO fetuses. Our findings clearly provide evidence that PRMT1 is essential for normal vascular formation during embryogenesis.

Free Research Field

生化学 分子生物学

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Published: 2018-03-22  

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