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Study of normal and pathological blood vessel morphogenesis in Flt1‐tdsRed BAC Tg mice
Author(s) -
Matsumoto Ken,
Azami Takuya,
Otsu Ayaka,
Takase Haruka,
Ishitobi Hiroyuki,
Tanaka Junko,
Miwa Yoshihiro,
Takahashi Satoru,
Ema Masatsugu
Publication year - 2012
Publication title -
genesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.093
H-Index - 110
eISSN - 1526-968X
pISSN - 1526-954X
DOI - 10.1002/dvg.22031
Subject(s) - angiogenesis , microbiology and biotechnology , biology , blood vessel , morphogenesis , filopodia , vascular endothelial growth factor , neovascularization , genetically modified mouse , vascular endothelial growth factor a , transgene , cancer research , endocrinology , gene , vegf receptors , actin , genetics
Blood vessel development and network patterning are controlled by several signaling molecules, including VEGF, FGF, TGF‐ß, and Ang‐1,2. Among these, the role of VEGF‐A signaling in vessel morphogenesis is best understood. The biological activity of VEGF‐A depends on its reaction with specific receptors Flt1 and Flk1. Roles of VEGF‐A signaling in endothelial cell proliferation, migration, survival, vascular permeability, and induction of tip cell filopodia have been reported. In this study, we have generated Flt1‐tdsRed BAC transgenic (Tg) mice to monitor Flt1 gene expression during vascular development. We show that tdsRed fluorescence is observed within blood vessels of adult mice and embryos, indicative of retinal angiogenesis and tumor angiogenesis. Flt1 expression recapitulated by Flt1‐tdsRed BAC Tg mice overlapped well with Flk1 , while Flt1 was expressed more abundantly in endothelial cells of large blood vessels such as dorsal aorta and presumptive stalk cells in retina, providing a unique model to study blood vessel development. genesis 50:561–571, 2012. © 2012 Wiley Periodicals, Inc.