Angiogenic inhibition reduces germinal matrix hemorrhage
The germinal matrix of premature infants is selectively vulnerable to hemorrhage within the first 48 h of life. To assess the role of vascular immaturity in germinal matrix hemorrhage (GMH), we evaluated germinal matrix angiogenesis in human fetuses and premature infants, as well as in premature rab...
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| Veröffentlicht in: | Nature medicine 2007-04, Vol.13 (4), p.477-485 |
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| creator | Ballabh, Praveen Xu, Hongmin Hu, Furong Braun, Alex Smith, Kira Rivera, Aracelie Lou, Nanhong Ungvari, Zoltan Goldman, Steven A Csiszar, Anna Nedergaard, Maiken |
| description | The germinal matrix of premature infants is selectively vulnerable to hemorrhage within the first 48 h of life. To assess the role of vascular immaturity in germinal matrix hemorrhage (GMH), we evaluated germinal matrix angiogenesis in human fetuses and premature infants, as well as in premature rabbit pups, and noted active vessel remodeling in all three. Vascular endothelial growth factor (VEGF), angiopoietin-2 and endothelial cell proliferation were present at consistently higher levels in the germinal matrix relative to the white matter anlagen and cortical mantle. On that basis, we asked whether prenatal treatment with either of two angiogenic inhibitors, the COX-2 inhibitor celecoxib, or the VEGFR2 inhibitor ZD6474, could suppress the incidence of GMH in premature rabbit pups. Celecoxib treatment decreased angiopoietin-2 and VEGF levels as well as germinal matrix endothelial proliferation. Furthermore, treatment with celecoxib or ZD6474 substantially decreased the incidence of GMH. Thus, by suppressing germinal matrix angiogenesis, prenatal celecoxib or ZD6474 treatment may be able to reduce both the incidence and severity of GMH in susceptible premature infants. |
| doi_str_mv | 10.1038/nm1558 |
| format | Article |
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To assess the role of vascular immaturity in germinal matrix hemorrhage (GMH), we evaluated germinal matrix angiogenesis in human fetuses and premature infants, as well as in premature rabbit pups, and noted active vessel remodeling in all three. Vascular endothelial growth factor (VEGF), angiopoietin-2 and endothelial cell proliferation were present at consistently higher levels in the germinal matrix relative to the white matter anlagen and cortical mantle. On that basis, we asked whether prenatal treatment with either of two angiogenic inhibitors, the COX-2 inhibitor celecoxib, or the VEGFR2 inhibitor ZD6474, could suppress the incidence of GMH in premature rabbit pups. Celecoxib treatment decreased angiopoietin-2 and VEGF levels as well as germinal matrix endothelial proliferation. Furthermore, treatment with celecoxib or ZD6474 substantially decreased the incidence of GMH. Thus, by suppressing germinal matrix angiogenesis, prenatal celecoxib or ZD6474 treatment may be able to reduce both the incidence and severity of GMH in susceptible premature infants.</description><identifier>ISSN: 1078-8956</identifier><identifier>EISSN: 1546-170X</identifier><identifier>DOI: 10.1038/nm1558</identifier><identifier>PMID: 17401377</identifier><language>eng</language><publisher>New York: Nature Publishing Group US</publisher><subject>Aborted Fetus ; Angiopoietin-2 - metabolism ; Animals ; Babies ; Biomedical and Life Sciences ; Biomedicine ; Blotting, Western ; Brain - blood supply ; Cancer Research ; Celecoxib ; Cell Proliferation - drug effects ; Cellular biology ; Cyclooxygenase 2 Inhibitors - pharmacology ; Endothelial Cells - drug effects ; Humans ; Immunohistochemistry ; Infant, Newborn ; Infant, Premature ; Infants ; Infectious Diseases ; Inhibitor drugs ; Intracranial Hemorrhages - prevention & control ; Metabolic Diseases ; Molecular Medicine ; Neovascularization, Physiologic - drug effects ; Neovascularization, Physiologic - physiology ; Neurosciences ; Piperidines - pharmacology ; Premature birth ; Pyrazoles - pharmacology ; Quinazolines - pharmacology ; Rabbits ; Sulfonamides - pharmacology ; Vascular Endothelial Growth Factor Receptor-2 - antagonists & inhibitors ; Veins & arteries</subject><ispartof>Nature medicine, 2007-04, Vol.13 (4), p.477-485</ispartof><rights>Springer Nature America, Inc. 2007</rights><rights>COPYRIGHT 2007 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Apr 2007</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c578t-ddd1d74bcb7aebc34e9d8f880d95970e5dd2de3ca8e657dbe9f9ab793cb71aa63</citedby><cites>FETCH-LOGICAL-c578t-ddd1d74bcb7aebc34e9d8f880d95970e5dd2de3ca8e657dbe9f9ab793cb71aa63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/nm1558$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/nm1558$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17401377$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ballabh, Praveen</creatorcontrib><creatorcontrib>Xu, Hongmin</creatorcontrib><creatorcontrib>Hu, Furong</creatorcontrib><creatorcontrib>Braun, Alex</creatorcontrib><creatorcontrib>Smith, Kira</creatorcontrib><creatorcontrib>Rivera, Aracelie</creatorcontrib><creatorcontrib>Lou, Nanhong</creatorcontrib><creatorcontrib>Ungvari, Zoltan</creatorcontrib><creatorcontrib>Goldman, Steven A</creatorcontrib><creatorcontrib>Csiszar, Anna</creatorcontrib><creatorcontrib>Nedergaard, Maiken</creatorcontrib><title>Angiogenic inhibition reduces germinal matrix hemorrhage</title><title>Nature medicine</title><addtitle>Nat Med</addtitle><addtitle>Nat Med</addtitle><description>The germinal matrix of premature infants is selectively vulnerable to hemorrhage within the first 48 h of life. To assess the role of vascular immaturity in germinal matrix hemorrhage (GMH), we evaluated germinal matrix angiogenesis in human fetuses and premature infants, as well as in premature rabbit pups, and noted active vessel remodeling in all three. Vascular endothelial growth factor (VEGF), angiopoietin-2 and endothelial cell proliferation were present at consistently higher levels in the germinal matrix relative to the white matter anlagen and cortical mantle. On that basis, we asked whether prenatal treatment with either of two angiogenic inhibitors, the COX-2 inhibitor celecoxib, or the VEGFR2 inhibitor ZD6474, could suppress the incidence of GMH in premature rabbit pups. Celecoxib treatment decreased angiopoietin-2 and VEGF levels as well as germinal matrix endothelial proliferation. Furthermore, treatment with celecoxib or ZD6474 substantially decreased the incidence of GMH. Thus, by suppressing germinal matrix angiogenesis, prenatal celecoxib or ZD6474 treatment may be able to reduce both the incidence and severity of GMH in susceptible premature infants.</description><subject>Aborted Fetus</subject><subject>Angiopoietin-2 - metabolism</subject><subject>Animals</subject><subject>Babies</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Blotting, Western</subject><subject>Brain - blood supply</subject><subject>Cancer Research</subject><subject>Celecoxib</subject><subject>Cell Proliferation - drug effects</subject><subject>Cellular biology</subject><subject>Cyclooxygenase 2 Inhibitors - pharmacology</subject><subject>Endothelial Cells - drug effects</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Infant, Newborn</subject><subject>Infant, Premature</subject><subject>Infants</subject><subject>Infectious Diseases</subject><subject>Inhibitor drugs</subject><subject>Intracranial Hemorrhages - 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metabolism</topic><topic>Animals</topic><topic>Babies</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Blotting, Western</topic><topic>Brain - blood supply</topic><topic>Cancer Research</topic><topic>Celecoxib</topic><topic>Cell Proliferation - drug effects</topic><topic>Cellular biology</topic><topic>Cyclooxygenase 2 Inhibitors - pharmacology</topic><topic>Endothelial Cells - drug effects</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Infant, Newborn</topic><topic>Infant, Premature</topic><topic>Infants</topic><topic>Infectious Diseases</topic><topic>Inhibitor drugs</topic><topic>Intracranial Hemorrhages - prevention & control</topic><topic>Metabolic Diseases</topic><topic>Molecular Medicine</topic><topic>Neovascularization, Physiologic - drug effects</topic><topic>Neovascularization, Physiologic - physiology</topic><topic>Neurosciences</topic><topic>Piperidines - pharmacology</topic><topic>Premature birth</topic><topic>Pyrazoles - 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Academic</collection><jtitle>Nature medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ballabh, Praveen</au><au>Xu, Hongmin</au><au>Hu, Furong</au><au>Braun, Alex</au><au>Smith, Kira</au><au>Rivera, Aracelie</au><au>Lou, Nanhong</au><au>Ungvari, Zoltan</au><au>Goldman, Steven A</au><au>Csiszar, Anna</au><au>Nedergaard, Maiken</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Angiogenic inhibition reduces germinal matrix hemorrhage</atitle><jtitle>Nature medicine</jtitle><stitle>Nat Med</stitle><addtitle>Nat Med</addtitle><date>2007-04-01</date><risdate>2007</risdate><volume>13</volume><issue>4</issue><spage>477</spage><epage>485</epage><pages>477-485</pages><issn>1078-8956</issn><eissn>1546-170X</eissn><abstract>The germinal matrix of premature infants is selectively vulnerable to hemorrhage within the first 48 h of life. To assess the role of vascular immaturity in germinal matrix hemorrhage (GMH), we evaluated germinal matrix angiogenesis in human fetuses and premature infants, as well as in premature rabbit pups, and noted active vessel remodeling in all three. Vascular endothelial growth factor (VEGF), angiopoietin-2 and endothelial cell proliferation were present at consistently higher levels in the germinal matrix relative to the white matter anlagen and cortical mantle. On that basis, we asked whether prenatal treatment with either of two angiogenic inhibitors, the COX-2 inhibitor celecoxib, or the VEGFR2 inhibitor ZD6474, could suppress the incidence of GMH in premature rabbit pups. Celecoxib treatment decreased angiopoietin-2 and VEGF levels as well as germinal matrix endothelial proliferation. Furthermore, treatment with celecoxib or ZD6474 substantially decreased the incidence of GMH. Thus, by suppressing germinal matrix angiogenesis, prenatal celecoxib or ZD6474 treatment may be able to reduce both the incidence and severity of GMH in susceptible premature infants.</abstract><cop>New York</cop><pub>Nature Publishing Group US</pub><pmid>17401377</pmid><doi>10.1038/nm1558</doi><tpages>9</tpages></addata></record> |
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| subjects | Aborted Fetus Angiopoietin-2 - metabolism Animals Babies Biomedical and Life Sciences Biomedicine Blotting, Western Brain - blood supply Cancer Research Celecoxib Cell Proliferation - drug effects Cellular biology Cyclooxygenase 2 Inhibitors - pharmacology Endothelial Cells - drug effects Humans Immunohistochemistry Infant, Newborn Infant, Premature Infants Infectious Diseases Inhibitor drugs Intracranial Hemorrhages - prevention & control Metabolic Diseases Molecular Medicine Neovascularization, Physiologic - drug effects Neovascularization, Physiologic - physiology Neurosciences Piperidines - pharmacology Premature birth Pyrazoles - pharmacology Quinazolines - pharmacology Rabbits Sulfonamides - pharmacology Vascular Endothelial Growth Factor Receptor-2 - antagonists & inhibitors Veins & arteries |
| title | Angiogenic inhibition reduces germinal matrix hemorrhage |
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