| Project/Area Number |
25670492
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Embryonic/Neonatal medicine
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| Research Institution | National Cardiovascular Center Research Institute (2014-2015)
Nara Medical University (2013) |
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Principal Investigator |
NAKAGAWA Osamu 国立研究開発法人国立循環器病研究センター, 研究所, 部長 (40283593)
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| Co-Investigator(Kenkyū-buntansha) |
SAKABE Masahide 奈良県立医科大学, 医学部, 助教 (00525983)
HAYASHI Hisaki 愛知医科大学, 医学部, 講師 (30533715)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 心血管発生 / 形態形成 / シグナル伝達 / 血管内皮 / 心血管形態形成 / 内皮細胞 / 循環器系 / 血管 / 心臓 / 発生分化 |
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| Outline of Final Research Achievements |
Mice that lack the ALK1/Acvrl1 receptor die before birth due to severe abnormalities of vascular formation, and the defects of ALK1-mediated signaling are implicated in the etiologies of human diseases including hereditary hemorrhagic telangiectasia and pulmonary arterial hypertension. We recently identified TMEM100, a gene encoding a previously uncharacterized transmembrane protein, to be an endothelium-enriched gene activated by the ALK1 signaling. Tmem100 null mice showed embryonic lethality due to the defects of vascular morphogenesis virtually identical to the abnormalities observed with the Acvrl1/Alk1 deficiency. In this study, we examined mechanisms of embryonic vascular expression and molecular functions of TMEM100 using various experimental techniques such as RNA measurement and transgenic mouse analysis. Further studies are ongoing in our laboratory to clarify the significance of TMEM100 in vascular development and disease.
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