| 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)
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| Budget Amount *help |
¥46,150,000 (Direct Cost: ¥35,500,000、Indirect Cost: ¥10,650,000)
Fiscal Year 2016: ¥11,700,000 (Direct Cost: ¥9,000,000、Indirect Cost: ¥2,700,000)
Fiscal Year 2015: ¥11,700,000 (Direct Cost: ¥9,000,000、Indirect Cost: ¥2,700,000)
Fiscal Year 2014: ¥10,790,000 (Direct Cost: ¥8,300,000、Indirect Cost: ¥2,490,000)
Fiscal Year 2013: ¥11,960,000 (Direct Cost: ¥9,200,000、Indirect Cost: ¥2,760,000)
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| 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.
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