Abnormal Angiogenesis in Foxo1 (Fkhr)-deficient Mice
Members of the Foxo family, Foxo1 ( Fkhr ), Foxo3 ( Fkhrl1 ), and Foxo4 (Afx), are mammalian homologs of daf-16 , which influences life span and energy metabolism in Caenorhabditis elegans . Mammalian FOXO proteins also play important roles in cell cycle arrest, apoptosis, stress resistance, and ene...
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| Veröffentlicht in: | The Journal of biological chemistry 2004-08, Vol.279 (33), p.34741-34749 |
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| container_title | The Journal of biological chemistry |
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| creator | Furuyama, Tatsuo Kitayama, Kazuko Shimoda, Yuri Ogawa, Minetaro Sone, Kiyoaki Yoshida-Araki, Kiyomi Hisatsune, Hiroshi Nishikawa, Shin-ichi Nakayama, Keiko Nakayama, Keiichi Ikeda, Kyoji Motoyama, Noboru Mori, Nozomu |
| description | Members of the Foxo family, Foxo1 ( Fkhr ), Foxo3 ( Fkhrl1 ), and Foxo4 (Afx), are mammalian homologs of daf-16 , which influences life span and energy metabolism in Caenorhabditis elegans . Mammalian FOXO proteins also play important roles in cell cycle arrest, apoptosis, stress resistance, and energy metabolism.
In this study, we generated Foxo1 -deficient mice to investigate the physiological role of FOXO1. The Foxo1 -deficient mice died around embryonic day 11 because of defects in the branchial arches and remarkably impaired vascular development
of embryos and yolk sacs. In vitro differentiation of embryonic stem cells demonstrated that endothelial cells derived from wild-type and Foxo1 -deficient embryonic stem cells were able to produce comparable numbers of colonies supported by a layer of OP9 stromal cells.
Although the morphology of the endothelial cell colonies was identical in both genotypes in the absence of exogenous vascular
endothelial growth factor (VEGF), Foxo1 -deficient endothelial cells showed a markedly different morphological response compared with wild-type endothelial cells
in the presence of exogenous VEGF. These results suggest that Foxo1 is essential to the ability of endothelial cells to respond properly to a high dose of VEGF, thereby playing a critical role
in normal vascular development. |
| doi_str_mv | 10.1074/jbc.M314214200 |
| format | Article |
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In this study, we generated Foxo1 -deficient mice to investigate the physiological role of FOXO1. The Foxo1 -deficient mice died around embryonic day 11 because of defects in the branchial arches and remarkably impaired vascular development
of embryos and yolk sacs. In vitro differentiation of embryonic stem cells demonstrated that endothelial cells derived from wild-type and Foxo1 -deficient embryonic stem cells were able to produce comparable numbers of colonies supported by a layer of OP9 stromal cells.
Although the morphology of the endothelial cell colonies was identical in both genotypes in the absence of exogenous vascular
endothelial growth factor (VEGF), Foxo1 -deficient endothelial cells showed a markedly different morphological response compared with wild-type endothelial cells
in the presence of exogenous VEGF. These results suggest that Foxo1 is essential to the ability of endothelial cells to respond properly to a high dose of VEGF, thereby playing a critical role
in normal vascular development.</description><identifier>ISSN: 0021-9258</identifier><identifier>EISSN: 1083-351X</identifier><identifier>DOI: 10.1074/jbc.M314214200</identifier><identifier>PMID: 15184386</identifier><language>eng</language><publisher>United States: American Society for Biochemistry and Molecular Biology</publisher><subject>Animals ; Antigens, CD ; Cadherins - metabolism ; Cell Differentiation ; Embryo, Mammalian - metabolism ; Endothelial Cells - metabolism ; Endothelium, Vascular - metabolism ; Forkhead Box Protein O1 ; Forkhead Transcription Factors ; Genotype ; Immunohistochemistry ; In Situ Hybridization ; Mice ; Mice, Transgenic ; Models, Genetic ; Neovascularization, Pathologic ; Reverse Transcriptase Polymerase Chain Reaction ; Time Factors ; Transcription Factors - genetics ; Transcription Factors - physiology ; Vascular Endothelial Growth Factor A - metabolism</subject><ispartof>The Journal of biological chemistry, 2004-08, Vol.279 (33), p.34741-34749</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c391t-7d2209510bd5013255769c60099082ccc53cb25f4ce90e7883b07377e89296de3</citedby><cites>FETCH-LOGICAL-c391t-7d2209510bd5013255769c60099082ccc53cb25f4ce90e7883b07377e89296de3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,27905,27906</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15184386$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Furuyama, Tatsuo</creatorcontrib><creatorcontrib>Kitayama, Kazuko</creatorcontrib><creatorcontrib>Shimoda, Yuri</creatorcontrib><creatorcontrib>Ogawa, Minetaro</creatorcontrib><creatorcontrib>Sone, Kiyoaki</creatorcontrib><creatorcontrib>Yoshida-Araki, Kiyomi</creatorcontrib><creatorcontrib>Hisatsune, Hiroshi</creatorcontrib><creatorcontrib>Nishikawa, Shin-ichi</creatorcontrib><creatorcontrib>Nakayama, Keiko</creatorcontrib><creatorcontrib>Nakayama, Keiichi</creatorcontrib><creatorcontrib>Ikeda, Kyoji</creatorcontrib><creatorcontrib>Motoyama, Noboru</creatorcontrib><creatorcontrib>Mori, Nozomu</creatorcontrib><title>Abnormal Angiogenesis in Foxo1 (Fkhr)-deficient Mice</title><title>The Journal of biological chemistry</title><addtitle>J Biol Chem</addtitle><description>Members of the Foxo family, Foxo1 ( Fkhr ), Foxo3 ( Fkhrl1 ), and Foxo4 (Afx), are mammalian homologs of daf-16 , which influences life span and energy metabolism in Caenorhabditis elegans . Mammalian FOXO proteins also play important roles in cell cycle arrest, apoptosis, stress resistance, and energy metabolism.
In this study, we generated Foxo1 -deficient mice to investigate the physiological role of FOXO1. The Foxo1 -deficient mice died around embryonic day 11 because of defects in the branchial arches and remarkably impaired vascular development
of embryos and yolk sacs. In vitro differentiation of embryonic stem cells demonstrated that endothelial cells derived from wild-type and Foxo1 -deficient embryonic stem cells were able to produce comparable numbers of colonies supported by a layer of OP9 stromal cells.
Although the morphology of the endothelial cell colonies was identical in both genotypes in the absence of exogenous vascular
endothelial growth factor (VEGF), Foxo1 -deficient endothelial cells showed a markedly different morphological response compared with wild-type endothelial cells
in the presence of exogenous VEGF. These results suggest that Foxo1 is essential to the ability of endothelial cells to respond properly to a high dose of VEGF, thereby playing a critical role
in normal vascular development.</description><subject>Animals</subject><subject>Antigens, CD</subject><subject>Cadherins - metabolism</subject><subject>Cell Differentiation</subject><subject>Embryo, Mammalian - metabolism</subject><subject>Endothelial Cells - metabolism</subject><subject>Endothelium, Vascular - metabolism</subject><subject>Forkhead Box Protein O1</subject><subject>Forkhead Transcription Factors</subject><subject>Genotype</subject><subject>Immunohistochemistry</subject><subject>In Situ Hybridization</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>Models, Genetic</subject><subject>Neovascularization, Pathologic</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>Time Factors</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - physiology</subject><subject>Vascular Endothelial Growth Factor A - metabolism</subject><issn>0021-9258</issn><issn>1083-351X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkD1PAkEQQDdGI4i2luYKY7Q4nNmP292SEFETiI0mdhtub4BF7k5vIeq_9wgklE4mmebNKx5jlwh9BC3vl7nvTwRK3i7AEesiGJEKhe_HrAvAMbVcmQ47i3EJ7UiLp6yDCo0UJusyOciruimnq2RQzUM9p4piiEmoklH9U2NyO_pYNHdpQbPgA1XrZBI8nbOT2XQV6WJ_e-xt9PA6fErHL4_Pw8E49cLiOtUF52AVQl4oQMGV0pn1GYC1YLj3XgmfczWTniyQNkbkoIXWZCy3WUGix2523s-m_tpQXLsyRE-r1bSiehNdlmmttur_QDTADaJswf4O9E0dY0Mz99mEctr8OgS3DeraoO4QtH242ps3eUnFAd8XbIHrHbAI88V3aMjlofYLKh3X1gnhhNQSxR8SUHlK</recordid><startdate>20040813</startdate><enddate>20040813</enddate><creator>Furuyama, Tatsuo</creator><creator>Kitayama, Kazuko</creator><creator>Shimoda, Yuri</creator><creator>Ogawa, Minetaro</creator><creator>Sone, Kiyoaki</creator><creator>Yoshida-Araki, Kiyomi</creator><creator>Hisatsune, Hiroshi</creator><creator>Nishikawa, Shin-ichi</creator><creator>Nakayama, Keiko</creator><creator>Nakayama, Keiichi</creator><creator>Ikeda, Kyoji</creator><creator>Motoyama, Noboru</creator><creator>Mori, Nozomu</creator><general>American Society for Biochemistry and Molecular Biology</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20040813</creationdate><title>Abnormal Angiogenesis in Foxo1 (Fkhr)-deficient Mice</title><author>Furuyama, Tatsuo ; Kitayama, Kazuko ; Shimoda, Yuri ; Ogawa, Minetaro ; Sone, Kiyoaki ; Yoshida-Araki, Kiyomi ; Hisatsune, Hiroshi ; Nishikawa, Shin-ichi ; Nakayama, Keiko ; Nakayama, Keiichi ; Ikeda, Kyoji ; Motoyama, Noboru ; Mori, Nozomu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c391t-7d2209510bd5013255769c60099082ccc53cb25f4ce90e7883b07377e89296de3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Animals</topic><topic>Antigens, CD</topic><topic>Cadherins - metabolism</topic><topic>Cell Differentiation</topic><topic>Embryo, Mammalian - metabolism</topic><topic>Endothelial Cells - metabolism</topic><topic>Endothelium, Vascular - metabolism</topic><topic>Forkhead Box Protein O1</topic><topic>Forkhead Transcription Factors</topic><topic>Genotype</topic><topic>Immunohistochemistry</topic><topic>In Situ Hybridization</topic><topic>Mice</topic><topic>Mice, Transgenic</topic><topic>Models, Genetic</topic><topic>Neovascularization, Pathologic</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>Time Factors</topic><topic>Transcription Factors - genetics</topic><topic>Transcription Factors - physiology</topic><topic>Vascular Endothelial Growth Factor A - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Furuyama, Tatsuo</creatorcontrib><creatorcontrib>Kitayama, Kazuko</creatorcontrib><creatorcontrib>Shimoda, Yuri</creatorcontrib><creatorcontrib>Ogawa, Minetaro</creatorcontrib><creatorcontrib>Sone, Kiyoaki</creatorcontrib><creatorcontrib>Yoshida-Araki, Kiyomi</creatorcontrib><creatorcontrib>Hisatsune, Hiroshi</creatorcontrib><creatorcontrib>Nishikawa, Shin-ichi</creatorcontrib><creatorcontrib>Nakayama, Keiko</creatorcontrib><creatorcontrib>Nakayama, Keiichi</creatorcontrib><creatorcontrib>Ikeda, Kyoji</creatorcontrib><creatorcontrib>Motoyama, Noboru</creatorcontrib><creatorcontrib>Mori, Nozomu</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>The Journal of biological chemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Furuyama, Tatsuo</au><au>Kitayama, Kazuko</au><au>Shimoda, Yuri</au><au>Ogawa, Minetaro</au><au>Sone, Kiyoaki</au><au>Yoshida-Araki, Kiyomi</au><au>Hisatsune, Hiroshi</au><au>Nishikawa, Shin-ichi</au><au>Nakayama, Keiko</au><au>Nakayama, Keiichi</au><au>Ikeda, Kyoji</au><au>Motoyama, Noboru</au><au>Mori, Nozomu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Abnormal Angiogenesis in Foxo1 (Fkhr)-deficient Mice</atitle><jtitle>The Journal of biological chemistry</jtitle><addtitle>J Biol Chem</addtitle><date>2004-08-13</date><risdate>2004</risdate><volume>279</volume><issue>33</issue><spage>34741</spage><epage>34749</epage><pages>34741-34749</pages><issn>0021-9258</issn><eissn>1083-351X</eissn><abstract>Members of the Foxo family, Foxo1 ( Fkhr ), Foxo3 ( Fkhrl1 ), and Foxo4 (Afx), are mammalian homologs of daf-16 , which influences life span and energy metabolism in Caenorhabditis elegans . Mammalian FOXO proteins also play important roles in cell cycle arrest, apoptosis, stress resistance, and energy metabolism.
In this study, we generated Foxo1 -deficient mice to investigate the physiological role of FOXO1. The Foxo1 -deficient mice died around embryonic day 11 because of defects in the branchial arches and remarkably impaired vascular development
of embryos and yolk sacs. In vitro differentiation of embryonic stem cells demonstrated that endothelial cells derived from wild-type and Foxo1 -deficient embryonic stem cells were able to produce comparable numbers of colonies supported by a layer of OP9 stromal cells.
Although the morphology of the endothelial cell colonies was identical in both genotypes in the absence of exogenous vascular
endothelial growth factor (VEGF), Foxo1 -deficient endothelial cells showed a markedly different morphological response compared with wild-type endothelial cells
in the presence of exogenous VEGF. These results suggest that Foxo1 is essential to the ability of endothelial cells to respond properly to a high dose of VEGF, thereby playing a critical role
in normal vascular development.</abstract><cop>United States</cop><pub>American Society for Biochemistry and Molecular Biology</pub><pmid>15184386</pmid><doi>10.1074/jbc.M314214200</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | The Journal of biological chemistry, 2004-08, Vol.279 (33), p.34741-34749 |
| issn | 0021-9258 1083-351X |
| language | eng |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Animals Antigens, CD Cadherins - metabolism Cell Differentiation Embryo, Mammalian - metabolism Endothelial Cells - metabolism Endothelium, Vascular - metabolism Forkhead Box Protein O1 Forkhead Transcription Factors Genotype Immunohistochemistry In Situ Hybridization Mice Mice, Transgenic Models, Genetic Neovascularization, Pathologic Reverse Transcriptase Polymerase Chain Reaction Time Factors Transcription Factors - genetics Transcription Factors - physiology Vascular Endothelial Growth Factor A - metabolism |
| title | Abnormal Angiogenesis in Foxo1 (Fkhr)-deficient Mice |
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