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Article: The PTEN/PI3K pathway governs normal vascular development and tumor angiogenesis

TitleThe PTEN/PI3K pathway governs normal vascular development and tumor angiogenesis
Authors
KeywordsPI3K
PTEN
Tumor angiogenesis
Cardiovasculogenesis
Endothelial cells
Issue Date2005
Citation
Genes and Development, 2005, v. 19, n. 17, p. 2054-2065 How to Cite?
AbstractPTEN is an important tumor suppressor gene. Hereditary mutation of PTEN causes tumor-susceptibility diseases such as Cowden disease. We used the Cre-loxP system to generate an endothelial cell-specific mutation of Pten (Tie2CrePten) in mice. Tie2CrePtenflox/+ mice displayed enhanced tumorigenesis due to an increase in angiogenesis driven by vascular growth factors. This effect was partially dependent on the PI3K subunits p85α and p110γ. In vitro, Tie2CrePtenflox/+ endothelial cells showed enhanced proliferation/migration. Tie2CrePtenflox/flox mice died before embryonic day 11.5 (E11.5) due to bleeding and cardiac failure caused by impaired recruitment of pericytes and vascular smooth muscle cells to blood vessels, and of cardiomyocytes to the endocardium. These phenotypes depend strongly on p110γ rather than on p85α and were associated with decreased expression of Ang-1, VCAM-1, connexin 40, and ephrinB2 but increased expression of Ang-2, VEGF-A, VEGFR1, and VEGFR2. Pten is thus indispensable for normal cardiovascular morphogenesis and post-natal angiogenesis, including tumor angiogenesis. © 2005 by Cold Spring Harbor Laboratory Press.
Persistent Identifierhttp://hdl.handle.net/10722/292535
ISSN
2023 Impact Factor: 7.5
2023 SCImago Journal Rankings: 5.015
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorHamada, Koichi-
dc.contributor.authorSasaki, Takehiko-
dc.contributor.authorKoni, Pandelakis A.-
dc.contributor.authorNatsui, Miyuki-
dc.contributor.authorKishimoto, Hiroyuki-
dc.contributor.authorSasaki, Junko-
dc.contributor.authorYajima, Nobuyuki-
dc.contributor.authorHorie, Yasuo-
dc.contributor.authorHasegawa, Go-
dc.contributor.authorNaito, Makoto-
dc.contributor.authorMiyazaki, Jun Ichi-
dc.contributor.authorSuda, Toshio-
dc.contributor.authorItoh, Hiroshi-
dc.contributor.authorNakao, Kazuwa-
dc.contributor.authorMak, Tak Wah-
dc.contributor.authorNakano, Toru-
dc.contributor.authorSuzuki, Akira-
dc.date.accessioned2020-11-17T14:56:41Z-
dc.date.available2020-11-17T14:56:41Z-
dc.date.issued2005-
dc.identifier.citationGenes and Development, 2005, v. 19, n. 17, p. 2054-2065-
dc.identifier.issn0890-9369-
dc.identifier.urihttp://hdl.handle.net/10722/292535-
dc.description.abstractPTEN is an important tumor suppressor gene. Hereditary mutation of PTEN causes tumor-susceptibility diseases such as Cowden disease. We used the Cre-loxP system to generate an endothelial cell-specific mutation of Pten (Tie2CrePten) in mice. Tie2CrePtenflox/+ mice displayed enhanced tumorigenesis due to an increase in angiogenesis driven by vascular growth factors. This effect was partially dependent on the PI3K subunits p85α and p110γ. In vitro, Tie2CrePtenflox/+ endothelial cells showed enhanced proliferation/migration. Tie2CrePtenflox/flox mice died before embryonic day 11.5 (E11.5) due to bleeding and cardiac failure caused by impaired recruitment of pericytes and vascular smooth muscle cells to blood vessels, and of cardiomyocytes to the endocardium. These phenotypes depend strongly on p110γ rather than on p85α and were associated with decreased expression of Ang-1, VCAM-1, connexin 40, and ephrinB2 but increased expression of Ang-2, VEGF-A, VEGFR1, and VEGFR2. Pten is thus indispensable for normal cardiovascular morphogenesis and post-natal angiogenesis, including tumor angiogenesis. © 2005 by Cold Spring Harbor Laboratory Press.-
dc.languageeng-
dc.relation.ispartofGenes and Development-
dc.subjectPI3K-
dc.subjectPTEN-
dc.subjectTumor angiogenesis-
dc.subjectCardiovasculogenesis-
dc.subjectEndothelial cells-
dc.titleThe PTEN/PI3K pathway governs normal vascular development and tumor angiogenesis-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1101/gad.1308805-
dc.identifier.pmid16107612-
dc.identifier.pmcidPMC1199575-
dc.identifier.scopuseid_2-s2.0-24344446438-
dc.identifier.volume19-
dc.identifier.issue17-
dc.identifier.spage2054-
dc.identifier.epage2065-
dc.identifier.isiWOS:000231630100010-
dc.identifier.issnl0890-9369-

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