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VEGF regulation of endothelial cell ...

Giles, Patrick Brian.

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VEGF regulation of endothelial cell survival, proliferation and lineage recruitment during embryonic vascular patterning.

Record Type:	Electronic resources : Monograph/item
Title/Author:	VEGF regulation of endothelial cell survival, proliferation and lineage recruitment during embryonic vascular patterning./
Author:	Giles, Patrick Brian.
Description:	146 p.
Notes:	Source: Dissertation Abstracts International, Volume: 65-04, Section: B, page: 1629.
Contained By:	Dissertation Abstracts International65-04B.
Subject:	Biology, Cell. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3129381
ISBN:	0496766417

VEGF regulation of endothelial cell survival, proliferation and lineage recruitment during embryonic vascular patterning.
Giles, Patrick Brian.

VEGF regulation of endothelial cell survival, proliferation and lineage recruitment during embryonic vascular patterning. - 146 p.

Source: Dissertation Abstracts International, Volume: 65-04, Section: B, page: 1629.

Thesis (Ph.D.)--Medical University of South Carolina, 2004.

A role for vascular endothelial growth factor (VEGF) as an in vivo regulator of vascular patterning was demonstrated by the ability of VEGF to convert the normally capillary-like pattern of blood vessels in the lateral networks of quail embryos into large vascular sinuses. That both normal large vessel morphogenesis and the VEGF-induced sinusoidal vessels are associated with increased endothelial cell density suggests that VEGF could be regulating the patterning of large blood vessels via its ability to control endothelial cell numbers/density. Work described herein evaluates potential mechanisms (apoptosis, proliferation and lineage recruitment) by which vascular endothelial growth factor (VEGF) could modulate endothelial cell numbers in the patterning of blood vessels. Our findings of negligible endothelial cell apoptosis associated with vasculogenesis, in either normal quail embryos or embryos in which the activity of endogenous VEGF was inhibited, suggest that apoptosis, and consequently VEGF's activity as a survival factor, is not relevant to early vascular morphogenesis. This finding is supported by studies in which we show that pharmacological inhibition of apoptosis in an in vitro model of vascular development did not have an effect on vascular morphogenesis. Proliferation as a mechanism by which VEGF could regulate endothelial cell numbers in vascular pattering was evaluated in vivo using antibodies to phosphohistone H3. In these studies, exogenous VEGF induced a 66% increase in endothelial cell proliferation in the lateral vascular networks during vascular hyperfusion. While these findings suggest a mitogenic role for VEGF during vasculogenesis, in vitro studies in which proliferation was inhibited by either mitomycin C or gamma-irradiation demonstrated that exogenous VEGF could induce a change in the patterning of blood vessels, i.e., vascular hyperfusion, independent of its mitogenic role. As vascular hyperfusion has been shown to be associated with an increase in endothelial cell density, we evaluated the intriguing possibility that VEGF signaling could be mediating the recruitment of new endothelial cell precursors from the mesoderm. Presented here are novel findings that VEGF was able to induce the ectopic formation of endothelial precursors from the newly gastrulated mesoderm, which is normally devoid of such cells.

ISBN: 0496766417Subjects--Topical Terms:

1017686
Biology, Cell.

VEGF regulation of endothelial cell survival, proliferation and lineage recruitment during embryonic vascular patterning.
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500 $a Source: Dissertation Abstracts International, Volume: 65-04, Section: B, page: 1629.
500 $a Director: Christopher J. Drake.
502 $a Thesis (Ph.D.)--Medical University of South Carolina, 2004.
520 $a A role for vascular endothelial growth factor (VEGF) as an in vivo regulator of vascular patterning was demonstrated by the ability of VEGF to convert the normally capillary-like pattern of blood vessels in the lateral networks of quail embryos into large vascular sinuses. That both normal large vessel morphogenesis and the VEGF-induced sinusoidal vessels are associated with increased endothelial cell density suggests that VEGF could be regulating the patterning of large blood vessels via its ability to control endothelial cell numbers/density. Work described herein evaluates potential mechanisms (apoptosis, proliferation and lineage recruitment) by which vascular endothelial growth factor (VEGF) could modulate endothelial cell numbers in the patterning of blood vessels. Our findings of negligible endothelial cell apoptosis associated with vasculogenesis, in either normal quail embryos or embryos in which the activity of endogenous VEGF was inhibited, suggest that apoptosis, and consequently VEGF's activity as a survival factor, is not relevant to early vascular morphogenesis. This finding is supported by studies in which we show that pharmacological inhibition of apoptosis in an in vitro model of vascular development did not have an effect on vascular morphogenesis. Proliferation as a mechanism by which VEGF could regulate endothelial cell numbers in vascular pattering was evaluated in vivo using antibodies to phosphohistone H3. In these studies, exogenous VEGF induced a 66% increase in endothelial cell proliferation in the lateral vascular networks during vascular hyperfusion. While these findings suggest a mitogenic role for VEGF during vasculogenesis, in vitro studies in which proliferation was inhibited by either mitomycin C or gamma-irradiation demonstrated that exogenous VEGF could induce a change in the patterning of blood vessels, i.e., vascular hyperfusion, independent of its mitogenic role. As vascular hyperfusion has been shown to be associated with an increase in endothelial cell density, we evaluated the intriguing possibility that VEGF signaling could be mediating the recruitment of new endothelial cell precursors from the mesoderm. Presented here are novel findings that VEGF was able to induce the ectopic formation of endothelial precursors from the newly gastrulated mesoderm, which is normally devoid of such cells.
590 $a School code: 0122.
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