Glomeruloid microvascular proliferation follows adenoviral vascular permeability factor/vascular endothelial growth factor-164 gene delivery

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Fältnamn	Indikatorer	Metadata
000		03047naa a2200337 4500
001		oai:DiVA.org:uu-197893
003		SwePub
008		130405s2001 \| \|\|\|\|\|\|\|\|\|\|\|000 \|\|eng\|
024	7	a https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-1978932 URI
024	7	a https://doi.org/10.1016/S0002-9440(10)64062-X2 DOI
040		a (SwePub)uu
041		a engb eng
042		9 SwePub
072	7	a ref2 swepub-contenttype
072	7	a art2 swepub-publicationtype
100	1	a Sundberg, Christianu Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts4 aut0 (Swepub:uu)chsun404
245	1 0	a Glomeruloid microvascular proliferation follows adenoviral vascular permeability factor/vascular endothelial growth factor-164 gene delivery
264	1	c 2001
338		a print2 rdacarrier
520		a Glomeruloid bodies are a defining histological feature of glioblastoma multiforme and some other tumors and vascular malformations. Little is known about their pathogenesis. We injected a nonreplicating adenoviral vector engineered to express vascular permeability factor/vascular endothelial growth factor-164 (VPF/VEGF(164)) into the ears of athymic mice. This vector infected local cells that strongly expressed VPF/VEGF(164) mRNA for 10 to 14 days, after which expression gradually declined. Locally expressed VPF/VEGF(164) induced an early increase in microvascular permeability, leading within 24 hours to edema and deposition of extravascular fibrin; in addition, many pre-existing microvessels enlarged to form thin-walled, pericyte-poor, "mother" vessels. Glomeruloid body precursors were first detected at 3 days as focal accumulations of rapidly proliferating cells in the endothelial lining of mother vessels, immediately adjacent to cells expressing VPF/VEGF(164). Initially, glomeruloid bodies were comprised of endothelial cells but subsequently pericytes and macrophages also participated. As they enlarged by endothelial cell and pericyte proliferation, glomeruloid bodies severely compromised mother vessel lumens and blood flow. Subsequently, as VPF/VEGF(164) expression declined, glomeruloid bodies devolved throughout a period of weeks by apoptosis and reorganization into normal-appearing microvessels. These results provide the first animal model for inducing glomeruloid bodies and indicate that VPF/VEGF(164) is sufficient for their induction and necessary for their maintenance.
700	1	a Nagy, J A4 aut
700	1	a Brown, L F4 aut
700	1	a Feng, D4 aut
700	1	a Eckelhoefer, I A4 aut
700	1	a Manseau, E J4 aut
700	1	a Dvorak, A M4 aut
700	1	a Dvorak, H F4 aut
710	2	a Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts4 org
773	0	t American Journal of Pathologyg 158:3, s. 1145-1160q 158:3<1145-1160x 0002-9440x 1525-2191
856	4 8	u https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-197893
856	4 8	u https://doi.org/10.1016/S0002-9440(10)64062-X

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Av författaren/redakt...: Sundberg, Christ ...; Nagy, J A; Brown, L F; Feng, D; Eckelhoefer, I A; Manseau, E J; visa fler...; Dvorak, A M; Dvorak, H F; visa färre...

Artiklar i publikationen: American Journal ...

Av lärosätet: Uppsala universitet

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