An important role of endothelial hairy-related transcription factors in mouse vascular development
Summary The Hairy‐related transcription factor family of Notch‐ and ALK1‐downstream transcriptional repressors, called Hrt/Hey/Hesr/Chf/Herp/Gridlock, has complementary and indispensable functions for vascular development. While mouse embryos null for either Hrt1/Hey1 or Hrt2/Hey2 did not show early...
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| Veröffentlicht in: | Genesis (New York, N.Y. : 2000) N.Y. : 2000), 2014-11, Vol.52 (11), p.897-906 |
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| creator | Morioka, Takashi Sakabe, Masahide Ioka, Tomoko Iguchi, Tomoko Mizuta, Ken Hattammaru, Miwa Sakai, Chihiro Itoh, Munehiro Sato, Genki E. Hashimoto, Aya Fujita, Masahide Okumura, Kazuki Araki, Mutsumi Xin, Mei Pedersen, Roger A. Utset, Manuel F. Kimura, Hiroshi Nakagawa, Osamu |
| description | Summary
The Hairy‐related transcription factor family of Notch‐ and ALK1‐downstream transcriptional repressors, called Hrt/Hey/Hesr/Chf/Herp/Gridlock, has complementary and indispensable functions for vascular development. While mouse embryos null for either Hrt1/Hey1 or Hrt2/Hey2 did not show early vascular phenotypes, Hrt1/Hey1; Hrt2/Hey2 double null mice (H1ko/H2ko) showed embryonic lethality with severe impairment of vascular morphogenesis. It remained unclear, however, whether Hrt/Hey functions are required in endothelial cells or vascular smooth muscle cells. In this study, we demonstrate that mice with endothelial‐specific deletion of Hrt2/Hey2 combined with global Hrt1/Hey1 deletion (H1ko/H2eko) show abnormal vascular morphogenesis and embryonic lethality. Their defects were characterized by the failure of vascular network formation in the yolk sac, abnormalities of embryonic vascular structures and impaired smooth muscle cell recruitment, and were virtually identical to the H1ko/H2ko phenotypes. Among signaling molecules implicated in vascular development, Robo4 expression was significantly increased and activation of Src family kinases was suppressed in endothelial cells of H1ko/H2eko embryos. The present study indicates an important role of Hrt1/Hey1 and Hrt2/Hey2 in endothelial cells during early vascular development, and further suggests involvement of Robo4 and Src family kinases in the mechanisms of embryonic vascular defects caused by the Hrt/Hey deficiency. genesis 52:897–906, 2014. © 2014 Wiley Periodicals, Inc. |
| doi_str_mv | 10.1002/dvg.22825 |
| format | Article |
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The Hairy‐related transcription factor family of Notch‐ and ALK1‐downstream transcriptional repressors, called Hrt/Hey/Hesr/Chf/Herp/Gridlock, has complementary and indispensable functions for vascular development. While mouse embryos null for either Hrt1/Hey1 or Hrt2/Hey2 did not show early vascular phenotypes, Hrt1/Hey1; Hrt2/Hey2 double null mice (H1ko/H2ko) showed embryonic lethality with severe impairment of vascular morphogenesis. It remained unclear, however, whether Hrt/Hey functions are required in endothelial cells or vascular smooth muscle cells. In this study, we demonstrate that mice with endothelial‐specific deletion of Hrt2/Hey2 combined with global Hrt1/Hey1 deletion (H1ko/H2eko) show abnormal vascular morphogenesis and embryonic lethality. Their defects were characterized by the failure of vascular network formation in the yolk sac, abnormalities of embryonic vascular structures and impaired smooth muscle cell recruitment, and were virtually identical to the H1ko/H2ko phenotypes. Among signaling molecules implicated in vascular development, Robo4 expression was significantly increased and activation of Src family kinases was suppressed in endothelial cells of H1ko/H2eko embryos. The present study indicates an important role of Hrt1/Hey1 and Hrt2/Hey2 in endothelial cells during early vascular development, and further suggests involvement of Robo4 and Src family kinases in the mechanisms of embryonic vascular defects caused by the Hrt/Hey deficiency. genesis 52:897–906, 2014. © 2014 Wiley Periodicals, Inc.</description><identifier>ISSN: 1526-954X</identifier><identifier>EISSN: 1526-968X</identifier><identifier>DOI: 10.1002/dvg.22825</identifier><identifier>PMID: 25264302</identifier><language>eng</language><publisher>United States: Blackwell Publishing Ltd</publisher><subject>Animals ; Basic Helix-Loop-Helix Transcription Factors - genetics ; Basic Helix-Loop-Helix Transcription Factors - metabolism ; Blotting, Western ; Cardiovascular System - embryology ; Endothelium - metabolism ; Gene Deletion ; Gene Expression Regulation, Developmental - genetics ; Gene Expression Regulation, Developmental - physiology ; Hrt/Hey ; Immunohistochemistry ; In Situ Hybridization ; Mice ; Morphogenesis - genetics ; Morphogenesis - physiology ; mouse embryo ; Nerve Tissue Proteins - metabolism ; Receptors, Immunologic - metabolism ; Repressor Proteins - genetics ; Repressor Proteins - metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Robo4 ; Signal Transduction - genetics ; Src family kinases ; vascular morphogenesis</subject><ispartof>Genesis (New York, N.Y. : 2000), 2014-11, Vol.52 (11), p.897-906</ispartof><rights>2014 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5655-1a4b62ef52db41038c02a5935d81918f5585763d8d7b5c94aef20b090468f5f03</citedby><cites>FETCH-LOGICAL-c5655-1a4b62ef52db41038c02a5935d81918f5585763d8d7b5c94aef20b090468f5f03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fdvg.22825$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fdvg.22825$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25264302$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Morioka, Takashi</creatorcontrib><creatorcontrib>Sakabe, Masahide</creatorcontrib><creatorcontrib>Ioka, Tomoko</creatorcontrib><creatorcontrib>Iguchi, Tomoko</creatorcontrib><creatorcontrib>Mizuta, Ken</creatorcontrib><creatorcontrib>Hattammaru, Miwa</creatorcontrib><creatorcontrib>Sakai, Chihiro</creatorcontrib><creatorcontrib>Itoh, Munehiro</creatorcontrib><creatorcontrib>Sato, Genki E.</creatorcontrib><creatorcontrib>Hashimoto, Aya</creatorcontrib><creatorcontrib>Fujita, Masahide</creatorcontrib><creatorcontrib>Okumura, Kazuki</creatorcontrib><creatorcontrib>Araki, Mutsumi</creatorcontrib><creatorcontrib>Xin, Mei</creatorcontrib><creatorcontrib>Pedersen, Roger A.</creatorcontrib><creatorcontrib>Utset, Manuel F.</creatorcontrib><creatorcontrib>Kimura, Hiroshi</creatorcontrib><creatorcontrib>Nakagawa, Osamu</creatorcontrib><title>An important role of endothelial hairy-related transcription factors in mouse vascular development</title><title>Genesis (New York, N.Y. : 2000)</title><addtitle>genesis</addtitle><description>Summary
The Hairy‐related transcription factor family of Notch‐ and ALK1‐downstream transcriptional repressors, called Hrt/Hey/Hesr/Chf/Herp/Gridlock, has complementary and indispensable functions for vascular development. While mouse embryos null for either Hrt1/Hey1 or Hrt2/Hey2 did not show early vascular phenotypes, Hrt1/Hey1; Hrt2/Hey2 double null mice (H1ko/H2ko) showed embryonic lethality with severe impairment of vascular morphogenesis. It remained unclear, however, whether Hrt/Hey functions are required in endothelial cells or vascular smooth muscle cells. In this study, we demonstrate that mice with endothelial‐specific deletion of Hrt2/Hey2 combined with global Hrt1/Hey1 deletion (H1ko/H2eko) show abnormal vascular morphogenesis and embryonic lethality. Their defects were characterized by the failure of vascular network formation in the yolk sac, abnormalities of embryonic vascular structures and impaired smooth muscle cell recruitment, and were virtually identical to the H1ko/H2ko phenotypes. Among signaling molecules implicated in vascular development, Robo4 expression was significantly increased and activation of Src family kinases was suppressed in endothelial cells of H1ko/H2eko embryos. The present study indicates an important role of Hrt1/Hey1 and Hrt2/Hey2 in endothelial cells during early vascular development, and further suggests involvement of Robo4 and Src family kinases in the mechanisms of embryonic vascular defects caused by the Hrt/Hey deficiency. genesis 52:897–906, 2014. © 2014 Wiley Periodicals, Inc.</description><subject>Animals</subject><subject>Basic Helix-Loop-Helix Transcription Factors - genetics</subject><subject>Basic Helix-Loop-Helix Transcription Factors - metabolism</subject><subject>Blotting, Western</subject><subject>Cardiovascular System - embryology</subject><subject>Endothelium - metabolism</subject><subject>Gene Deletion</subject><subject>Gene Expression Regulation, Developmental - genetics</subject><subject>Gene Expression Regulation, Developmental - physiology</subject><subject>Hrt/Hey</subject><subject>Immunohistochemistry</subject><subject>In Situ Hybridization</subject><subject>Mice</subject><subject>Morphogenesis - genetics</subject><subject>Morphogenesis - physiology</subject><subject>mouse embryo</subject><subject>Nerve Tissue Proteins - metabolism</subject><subject>Receptors, Immunologic - metabolism</subject><subject>Repressor Proteins - genetics</subject><subject>Repressor Proteins - metabolism</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>Robo4</subject><subject>Signal Transduction - genetics</subject><subject>Src family kinases</subject><subject>vascular morphogenesis</subject><issn>1526-954X</issn><issn>1526-968X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kE1v1DAQhi0EoqVw4A8gS1zgkNYfceIcq0K3SBUg8dEVF8uJJ9TFsVPbWdh_j2G7PSBxmpHmeV-NHoSeU3JMCWEnZvP9mDHJxAN0SAVrqq6R64f7XdTrA_QkpRtCiJCMPUYHrBxqTtgh6k89ttMcYtY-4xgc4DBi8Cbka3BWO3ytbdxWEZzOYHCO2qch2jnb4PGohxxiwtbjKSwJ8EanYXE6YgMbcGGewOen6NGoXYJnd_MIfTl_-_nsorr8sHp3dnpZDaIRoqK67hsGo2CmrynhciBMi44LI2lH5SiEFG3DjTRtL4au1jAy0pOO1E05joQfoVe73jmG2wVSVpNNAzinPZTnFG2KIi4bURf05T_oTViiL98VSnStbDvCC_V6Rw0xpBRhVHO0k45bRYn6I14V8eqv-MK-uGtc-gnMPbk3XYCTHfDTOtj-v0m9-braV1a7hE0Zft0ndPyhmpa3Ql29X6mrjxfdt0-rtTrnvwEVyJxR</recordid><startdate>201411</startdate><enddate>201411</enddate><creator>Morioka, Takashi</creator><creator>Sakabe, Masahide</creator><creator>Ioka, Tomoko</creator><creator>Iguchi, Tomoko</creator><creator>Mizuta, Ken</creator><creator>Hattammaru, Miwa</creator><creator>Sakai, Chihiro</creator><creator>Itoh, Munehiro</creator><creator>Sato, Genki E.</creator><creator>Hashimoto, Aya</creator><creator>Fujita, Masahide</creator><creator>Okumura, Kazuki</creator><creator>Araki, Mutsumi</creator><creator>Xin, Mei</creator><creator>Pedersen, Roger A.</creator><creator>Utset, Manuel F.</creator><creator>Kimura, Hiroshi</creator><creator>Nakagawa, Osamu</creator><general>Blackwell Publishing Ltd</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</scope><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>7QL</scope><scope>7QP</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>201411</creationdate><title>An important role of endothelial hairy-related transcription factors in mouse vascular development</title><author>Morioka, Takashi ; Sakabe, Masahide ; Ioka, Tomoko ; Iguchi, Tomoko ; Mizuta, Ken ; Hattammaru, Miwa ; Sakai, Chihiro ; Itoh, Munehiro ; Sato, Genki E. ; Hashimoto, Aya ; Fujita, Masahide ; Okumura, Kazuki ; Araki, Mutsumi ; Xin, Mei ; Pedersen, Roger A. ; Utset, Manuel F. ; Kimura, Hiroshi ; Nakagawa, Osamu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5655-1a4b62ef52db41038c02a5935d81918f5585763d8d7b5c94aef20b090468f5f03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Animals</topic><topic>Basic Helix-Loop-Helix Transcription Factors - genetics</topic><topic>Basic Helix-Loop-Helix Transcription Factors - metabolism</topic><topic>Blotting, Western</topic><topic>Cardiovascular System - embryology</topic><topic>Endothelium - metabolism</topic><topic>Gene Deletion</topic><topic>Gene Expression Regulation, Developmental - genetics</topic><topic>Gene Expression Regulation, Developmental - physiology</topic><topic>Hrt/Hey</topic><topic>Immunohistochemistry</topic><topic>In Situ Hybridization</topic><topic>Mice</topic><topic>Morphogenesis - genetics</topic><topic>Morphogenesis - physiology</topic><topic>mouse embryo</topic><topic>Nerve Tissue Proteins - metabolism</topic><topic>Receptors, Immunologic - metabolism</topic><topic>Repressor Proteins - genetics</topic><topic>Repressor Proteins - metabolism</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>Robo4</topic><topic>Signal Transduction - genetics</topic><topic>Src family kinases</topic><topic>vascular morphogenesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Morioka, Takashi</creatorcontrib><creatorcontrib>Sakabe, Masahide</creatorcontrib><creatorcontrib>Ioka, Tomoko</creatorcontrib><creatorcontrib>Iguchi, Tomoko</creatorcontrib><creatorcontrib>Mizuta, Ken</creatorcontrib><creatorcontrib>Hattammaru, Miwa</creatorcontrib><creatorcontrib>Sakai, Chihiro</creatorcontrib><creatorcontrib>Itoh, Munehiro</creatorcontrib><creatorcontrib>Sato, Genki E.</creatorcontrib><creatorcontrib>Hashimoto, Aya</creatorcontrib><creatorcontrib>Fujita, Masahide</creatorcontrib><creatorcontrib>Okumura, Kazuki</creatorcontrib><creatorcontrib>Araki, Mutsumi</creatorcontrib><creatorcontrib>Xin, Mei</creatorcontrib><creatorcontrib>Pedersen, Roger A.</creatorcontrib><creatorcontrib>Utset, Manuel F.</creatorcontrib><creatorcontrib>Kimura, Hiroshi</creatorcontrib><creatorcontrib>Nakagawa, Osamu</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Genesis (New York, N.Y. : 2000)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Morioka, Takashi</au><au>Sakabe, Masahide</au><au>Ioka, Tomoko</au><au>Iguchi, Tomoko</au><au>Mizuta, Ken</au><au>Hattammaru, Miwa</au><au>Sakai, Chihiro</au><au>Itoh, Munehiro</au><au>Sato, Genki E.</au><au>Hashimoto, Aya</au><au>Fujita, Masahide</au><au>Okumura, Kazuki</au><au>Araki, Mutsumi</au><au>Xin, Mei</au><au>Pedersen, Roger A.</au><au>Utset, Manuel F.</au><au>Kimura, Hiroshi</au><au>Nakagawa, Osamu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>An important role of endothelial hairy-related transcription factors in mouse vascular development</atitle><jtitle>Genesis (New York, N.Y. : 2000)</jtitle><addtitle>genesis</addtitle><date>2014-11</date><risdate>2014</risdate><volume>52</volume><issue>11</issue><spage>897</spage><epage>906</epage><pages>897-906</pages><issn>1526-954X</issn><eissn>1526-968X</eissn><abstract>Summary
The Hairy‐related transcription factor family of Notch‐ and ALK1‐downstream transcriptional repressors, called Hrt/Hey/Hesr/Chf/Herp/Gridlock, has complementary and indispensable functions for vascular development. While mouse embryos null for either Hrt1/Hey1 or Hrt2/Hey2 did not show early vascular phenotypes, Hrt1/Hey1; Hrt2/Hey2 double null mice (H1ko/H2ko) showed embryonic lethality with severe impairment of vascular morphogenesis. It remained unclear, however, whether Hrt/Hey functions are required in endothelial cells or vascular smooth muscle cells. In this study, we demonstrate that mice with endothelial‐specific deletion of Hrt2/Hey2 combined with global Hrt1/Hey1 deletion (H1ko/H2eko) show abnormal vascular morphogenesis and embryonic lethality. Their defects were characterized by the failure of vascular network formation in the yolk sac, abnormalities of embryonic vascular structures and impaired smooth muscle cell recruitment, and were virtually identical to the H1ko/H2ko phenotypes. Among signaling molecules implicated in vascular development, Robo4 expression was significantly increased and activation of Src family kinases was suppressed in endothelial cells of H1ko/H2eko embryos. The present study indicates an important role of Hrt1/Hey1 and Hrt2/Hey2 in endothelial cells during early vascular development, and further suggests involvement of Robo4 and Src family kinases in the mechanisms of embryonic vascular defects caused by the Hrt/Hey deficiency. genesis 52:897–906, 2014. © 2014 Wiley Periodicals, Inc.</abstract><cop>United States</cop><pub>Blackwell Publishing Ltd</pub><pmid>25264302</pmid><doi>10.1002/dvg.22825</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Basic Helix-Loop-Helix Transcription Factors - genetics Basic Helix-Loop-Helix Transcription Factors - metabolism Blotting, Western Cardiovascular System - embryology Endothelium - metabolism Gene Deletion Gene Expression Regulation, Developmental - genetics Gene Expression Regulation, Developmental - physiology Hrt/Hey Immunohistochemistry In Situ Hybridization Mice Morphogenesis - genetics Morphogenesis - physiology mouse embryo Nerve Tissue Proteins - metabolism Receptors, Immunologic - metabolism Repressor Proteins - genetics Repressor Proteins - metabolism Reverse Transcriptase Polymerase Chain Reaction Robo4 Signal Transduction - genetics Src family kinases vascular morphogenesis |
| title | An important role of endothelial hairy-related transcription factors in mouse vascular development |
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