Suppression of Sproutys has a therapeutic effect for a mouse model of ischemia by enhancing angiogenesis
Sprouty proteins (Sproutys) inhibit receptor tyrosine kinase signaling and control various aspects of branching morphogenesis. In this study, we examined the physiological function of Sproutys in angiogenesis, using gene targeting and short-hairpin RNA (shRNA) knockdown strategies. Sprouty2 and Spro...
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| creator | Taniguchi, Koji Sasaki, Ken-ichiro Watari, Kousuke Yasukawa, Hideo Imaizumi, Tsutomu Ayada, Toranoshin Okamoto, Fuyuki Ishizaki, Takuma Kato, Reiko Kohno, Ri-ichiro Kimura, Hiroshi Sato, Yasufumi Ono, Mayumi Yonemitsu, Yoshikazu Yoshimura, Akihiko |
| description | Sprouty proteins (Sproutys) inhibit receptor tyrosine kinase signaling and control various aspects of branching morphogenesis. In this study, we examined the physiological function of Sproutys in angiogenesis, using gene targeting and short-hairpin RNA (shRNA) knockdown strategies. Sprouty2 and Sprouty4 double knockout (KO) (DKO) mice were embryonic-lethal around E12.5 due to cardiovascular defects. The number of peripheral blood vessels, but not that of lymphatic vessels, was increased in Sprouty4 KO mice compared with wild-type (WT) mice. Sprouty4 KO mice were more resistant to hind limb ischemia and soft tissue ischemia than WT mice were, because Sprouty4 deficiency causes accelerated neovascularization. Moreover, suppression of Sprouty2 and Sprouty4 expression in vivo by shRNA targeting accelerated angiogenesis and has a therapeutic effect in a mouse model of hind limb ischemia. These data suggest that Sproutys are physiologically important negative regulators of angiogenesis in vivo and novel therapeutic targets for treating peripheral ischemic diseases. |
| doi_str_mv | 10.1371/journal.pone.0005467 |
| format | Article |
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In this study, we examined the physiological function of Sproutys in angiogenesis, using gene targeting and short-hairpin RNA (shRNA) knockdown strategies. Sprouty2 and Sprouty4 double knockout (KO) (DKO) mice were embryonic-lethal around E12.5 due to cardiovascular defects. The number of peripheral blood vessels, but not that of lymphatic vessels, was increased in Sprouty4 KO mice compared with wild-type (WT) mice. Sprouty4 KO mice were more resistant to hind limb ischemia and soft tissue ischemia than WT mice were, because Sprouty4 deficiency causes accelerated neovascularization. Moreover, suppression of Sprouty2 and Sprouty4 expression in vivo by shRNA targeting accelerated angiogenesis and has a therapeutic effect in a mouse model of hind limb ischemia. These data suggest that Sproutys are physiologically important negative regulators of angiogenesis in vivo and novel therapeutic targets for treating peripheral ischemic diseases.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0005467</identifier><identifier>PMID: 19424491</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adaptor Proteins, Signal Transducing ; Angiogenesis ; Animals ; Atherosclerosis ; Blood vessels ; Blood Vessels - pathology ; Cardiovascular Disorders ; Cardiovascular Disorders/Peripheral Vascular Disease ; Cell Biology ; Cell Biology/Cell Signaling ; Cell growth ; Comparative analysis ; Cornea - blood supply ; Diabetic retinopathy ; Disease Models, Animal ; Drosophila ; Embryos ; Fibroblasts ; Gene targeting ; Gene therapy ; Health aspects ; Hindlimb - blood supply ; Immunology ; Insects ; Internal medicine ; Intracellular Signaling Peptides and Proteins ; Ischemia ; Ischemia - physiopathology ; Ischemia - therapy ; Kinases ; Localization ; Lymphatic system ; Lymphatic Vessels - pathology ; Medicine ; Membrane Proteins - deficiency ; Membrane Proteins - metabolism ; Mice ; Mice, Knockout ; Morphogenesis ; Neovascularization ; Neovascularization, Physiologic ; Nerve Tissue Proteins - deficiency ; Nerve Tissue Proteins - metabolism ; Pathology ; Peripheral blood ; Pharmaceutical sciences ; Physiological aspects ; Physiology ; Protein-tyrosine kinase receptors ; Proteins ; Regulation ; Ribonucleic acid ; RNA ; RNA, Small Interfering - metabolism ; Rodents ; Smooth muscle ; Tyrosine ; Vascular endothelial growth factor ; Vascularization</subject><ispartof>PloS one, 2009-05, Vol.4 (5), p.e5467-e5467</ispartof><rights>COPYRIGHT 2009 Public Library of Science</rights><rights>2009 Taniguchi et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Taniguchi et al. 2009</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c756t-125b0fe28e806230398dc5436037b4be3749e55f707ccd0faeacdc29c6feebfc3</citedby><cites>FETCH-LOGICAL-c756t-125b0fe28e806230398dc5436037b4be3749e55f707ccd0faeacdc29c6feebfc3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2674940/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2674940/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79342,79343</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19424491$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Taniguchi, Koji</creatorcontrib><creatorcontrib>Sasaki, Ken-ichiro</creatorcontrib><creatorcontrib>Watari, Kousuke</creatorcontrib><creatorcontrib>Yasukawa, Hideo</creatorcontrib><creatorcontrib>Imaizumi, Tsutomu</creatorcontrib><creatorcontrib>Ayada, Toranoshin</creatorcontrib><creatorcontrib>Okamoto, Fuyuki</creatorcontrib><creatorcontrib>Ishizaki, Takuma</creatorcontrib><creatorcontrib>Kato, Reiko</creatorcontrib><creatorcontrib>Kohno, Ri-ichiro</creatorcontrib><creatorcontrib>Kimura, Hiroshi</creatorcontrib><creatorcontrib>Sato, Yasufumi</creatorcontrib><creatorcontrib>Ono, Mayumi</creatorcontrib><creatorcontrib>Yonemitsu, Yoshikazu</creatorcontrib><creatorcontrib>Yoshimura, Akihiko</creatorcontrib><title>Suppression of Sproutys has a therapeutic effect for a mouse model of ischemia by enhancing angiogenesis</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Sprouty proteins (Sproutys) inhibit receptor tyrosine kinase signaling and control various aspects of branching morphogenesis. In this study, we examined the physiological function of Sproutys in angiogenesis, using gene targeting and short-hairpin RNA (shRNA) knockdown strategies. Sprouty2 and Sprouty4 double knockout (KO) (DKO) mice were embryonic-lethal around E12.5 due to cardiovascular defects. The number of peripheral blood vessels, but not that of lymphatic vessels, was increased in Sprouty4 KO mice compared with wild-type (WT) mice. Sprouty4 KO mice were more resistant to hind limb ischemia and soft tissue ischemia than WT mice were, because Sprouty4 deficiency causes accelerated neovascularization. Moreover, suppression of Sprouty2 and Sprouty4 expression in vivo by shRNA targeting accelerated angiogenesis and has a therapeutic effect in a mouse model of hind limb ischemia. These data suggest that Sproutys are physiologically important negative regulators of angiogenesis in vivo and novel therapeutic targets for treating peripheral ischemic diseases.</description><subject>Adaptor Proteins, Signal Transducing</subject><subject>Angiogenesis</subject><subject>Animals</subject><subject>Atherosclerosis</subject><subject>Blood vessels</subject><subject>Blood Vessels - pathology</subject><subject>Cardiovascular Disorders</subject><subject>Cardiovascular Disorders/Peripheral Vascular Disease</subject><subject>Cell Biology</subject><subject>Cell Biology/Cell Signaling</subject><subject>Cell growth</subject><subject>Comparative analysis</subject><subject>Cornea - blood supply</subject><subject>Diabetic retinopathy</subject><subject>Disease Models, Animal</subject><subject>Drosophila</subject><subject>Embryos</subject><subject>Fibroblasts</subject><subject>Gene targeting</subject><subject>Gene therapy</subject><subject>Health aspects</subject><subject>Hindlimb - blood supply</subject><subject>Immunology</subject><subject>Insects</subject><subject>Internal medicine</subject><subject>Intracellular Signaling Peptides and Proteins</subject><subject>Ischemia</subject><subject>Ischemia - physiopathology</subject><subject>Ischemia - therapy</subject><subject>Kinases</subject><subject>Localization</subject><subject>Lymphatic system</subject><subject>Lymphatic Vessels - pathology</subject><subject>Medicine</subject><subject>Membrane Proteins - deficiency</subject><subject>Membrane Proteins - metabolism</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Morphogenesis</subject><subject>Neovascularization</subject><subject>Neovascularization, Physiologic</subject><subject>Nerve Tissue Proteins - deficiency</subject><subject>Nerve Tissue Proteins - metabolism</subject><subject>Pathology</subject><subject>Peripheral blood</subject><subject>Pharmaceutical sciences</subject><subject>Physiological aspects</subject><subject>Physiology</subject><subject>Protein-tyrosine kinase receptors</subject><subject>Proteins</subject><subject>Regulation</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>RNA, Small Interfering - metabolism</subject><subject>Rodents</subject><subject>Smooth muscle</subject><subject>Tyrosine</subject><subject>Vascular endothelial growth 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of Sproutys has a therapeutic effect for a mouse model of ischemia by enhancing angiogenesis</title><author>Taniguchi, Koji ; Sasaki, Ken-ichiro ; Watari, Kousuke ; Yasukawa, Hideo ; Imaizumi, Tsutomu ; Ayada, Toranoshin ; Okamoto, Fuyuki ; Ishizaki, Takuma ; Kato, Reiko ; Kohno, Ri-ichiro ; Kimura, Hiroshi ; Sato, Yasufumi ; Ono, Mayumi ; Yonemitsu, Yoshikazu ; Yoshimura, Akihiko</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c756t-125b0fe28e806230398dc5436037b4be3749e55f707ccd0faeacdc29c6feebfc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Adaptor Proteins, Signal Transducing</topic><topic>Angiogenesis</topic><topic>Animals</topic><topic>Atherosclerosis</topic><topic>Blood vessels</topic><topic>Blood Vessels - pathology</topic><topic>Cardiovascular Disorders</topic><topic>Cardiovascular Disorders/Peripheral Vascular Disease</topic><topic>Cell 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One</addtitle><date>2009-05-08</date><risdate>2009</risdate><volume>4</volume><issue>5</issue><spage>e5467</spage><epage>e5467</epage><pages>e5467-e5467</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Sprouty proteins (Sproutys) inhibit receptor tyrosine kinase signaling and control various aspects of branching morphogenesis. In this study, we examined the physiological function of Sproutys in angiogenesis, using gene targeting and short-hairpin RNA (shRNA) knockdown strategies. Sprouty2 and Sprouty4 double knockout (KO) (DKO) mice were embryonic-lethal around E12.5 due to cardiovascular defects. The number of peripheral blood vessels, but not that of lymphatic vessels, was increased in Sprouty4 KO mice compared with wild-type (WT) mice. Sprouty4 KO mice were more resistant to hind limb ischemia and soft tissue ischemia than WT mice were, because Sprouty4 deficiency causes accelerated neovascularization. Moreover, suppression of Sprouty2 and Sprouty4 expression in vivo by shRNA targeting accelerated angiogenesis and has a therapeutic effect in a mouse model of hind limb ischemia. These data suggest that Sproutys are physiologically important negative regulators of angiogenesis in vivo and novel therapeutic targets for treating peripheral ischemic diseases.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>19424491</pmid><doi>10.1371/journal.pone.0005467</doi><tpages>e5467</tpages><oa>free_for_read</oa></addata></record> |
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| recordid | cdi_plos_journals_1290141170 |
| source | Public Library of Science (PLoS) Journals Open Access; MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Adaptor Proteins, Signal Transducing Angiogenesis Animals Atherosclerosis Blood vessels Blood Vessels - pathology Cardiovascular Disorders Cardiovascular Disorders/Peripheral Vascular Disease Cell Biology Cell Biology/Cell Signaling Cell growth Comparative analysis Cornea - blood supply Diabetic retinopathy Disease Models, Animal Drosophila Embryos Fibroblasts Gene targeting Gene therapy Health aspects Hindlimb - blood supply Immunology Insects Internal medicine Intracellular Signaling Peptides and Proteins Ischemia Ischemia - physiopathology Ischemia - therapy Kinases Localization Lymphatic system Lymphatic Vessels - pathology Medicine Membrane Proteins - deficiency Membrane Proteins - metabolism Mice Mice, Knockout Morphogenesis Neovascularization Neovascularization, Physiologic Nerve Tissue Proteins - deficiency Nerve Tissue Proteins - metabolism Pathology Peripheral blood Pharmaceutical sciences Physiological aspects Physiology Protein-tyrosine kinase receptors Proteins Regulation Ribonucleic acid RNA RNA, Small Interfering - metabolism Rodents Smooth muscle Tyrosine Vascular endothelial growth factor Vascularization |
| title | Suppression of Sproutys has a therapeutic effect for a mouse model of ischemia by enhancing angiogenesis |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-07T01%3A12%3A49IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Suppression%20of%20Sproutys%20has%20a%20therapeutic%20effect%20for%20a%20mouse%20model%20of%20ischemia%20by%20enhancing%20angiogenesis&rft.jtitle=PloS%20one&rft.au=Taniguchi,%20Koji&rft.date=2009-05-08&rft.volume=4&rft.issue=5&rft.spage=e5467&rft.epage=e5467&rft.pages=e5467-e5467&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0005467&rft_dat=%3Cgale_plos_%3EA473179663%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1290141170&rft_id=info:pmid/19424491&rft_galeid=A473179663&rft_doaj_id=oai_doaj_org_article_2a2cd5ceac8f4358b3b89b73a41a68e7&rfr_iscdi=true |