2002 Fiscal Year Final Research Report Summary
Function of Dell in Embryonic Development
| Project/Area Number |
13670027
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General anatomy (including Histology/Embryology)
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| Research Institution | Nihon University School of Medicine |
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Principal Investigator |
HIDAI Chiaki Nihon University, School of Medicine, Lecturer., 医学部, 講師 (70228732)
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| Co-Investigator(Kenkyū-buntansha) |
KAWANA Masatoshi Tokyo Women's Medical University, School of Medicine Assistant Professor, 医学部, 助教授 (20152978)
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| Project Period (FY) |
2001 – 2002
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| Keywords | Endothelia cell / Development / Angiogenesis |
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| Research Abstract |
Vascular remodeling is an essential process that allows the primary vascular plexus to develop into matured vasculature during embryonic development. Gene-targeting experiments have revealed that such remodeling is regulated by the products of several different genes. These include secreted molecules, receptor tyrosine kinases, and transcription factors. In mutant mice lacking these molecules, the primary vascular plexus fails to assemble into large vessels during development. Unfortunately, these 'loss of function' experiments do not advance our understanding of how vascular remodeling controls branching morphogenesis during development. Dell is an extracellular matrix protein that is exclusively expressed in embryonic endothelial cells. To investigate Dell function in developing embryos, we used a cytomegalovirus enhancer seguence to generate Dell overexpression mice, using. In transgenic mice, the total vascular bed was decreased in the alimentary tracts because of accelerated vascular remodeling at mid stage gestation. In addition to the quantitative change, overexpression of Dell reorganized vascular branching patterns, resulting in dendritic vessels. The present study indicates that Dell overexpression accelerates vascular remodeling and causes changes in branching morphogenesis during embryonic development
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