Pathological Neovascularization Is Reduced by Inactivation of ADAM17 in Endothelial Cells but Not in Pericytes
RATIONALE:Pathological neovascularization is a critical component of diseases such as proliferative retinopathies, cancer and rheumatoid arthritis, yet much remains to be learned about the underlying causes. Previous studies showed that vascular endothelial growth factor (VEGF)-A activates the membr...
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| Veröffentlicht in: | Circulation research 2010-03, Vol.106 (5), p.932-940 |
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| creator | Weskamp, Gisela Mendelson, Karen Swendeman, Steve Le Gall, Sylvain Ma, Yan Lyman, Stephen Hinoki, Akinari Eguchi, Satoru Guaiquil, Victor Horiuchi, Keisuke Blobel, Carl P |
| description | RATIONALE:Pathological neovascularization is a critical component of diseases such as proliferative retinopathies, cancer and rheumatoid arthritis, yet much remains to be learned about the underlying causes. Previous studies showed that vascular endothelial growth factor (VEGF)-A activates the membrane-anchored metalloproteinase ADAM17 (a disintegrin and metalloproteinase 17) in endothelial cells, thereby stimulating crosstalk between VEGF receptor 2 and extracellular signal-regulated kinase. These findings raised interesting questions about the role of ADAM17 in angiogenesis and neovascularization in vivo.
OBJECTIVE:The objective of this study was to inactivate ADAM17 in endothelial cells or in pericytes to determine how this affects developmental angiogenesis, pathological retinal neovascularization and heterotopic tumor growth.
METHODS AND RESULTS:We generated animals in which floxed ADAM17 was removed by Tie2-Cre in endothelial cells, or by smooth muscle (sm) Cre in smooth muscle cells and pericytes. There were no evident developmental defects in either conditional knockout strain, but pathological retinal neovascularization and growth of heterotopically injected tumor cells was reduced in Adam17flox/flox/Tie2-Cre mice, although not in Adam17flox/flox/sm-Cre mice. Moreover, lack of ADAM17 in endothelial cells decreased ex vivo chord formation, and this could be largely restored by addition of the ADAM17 substrate HB-EGF (heparin-binding epidermal growth factor-like growth factor). Finally we found that ADAM17 is important for the VEGF receptor 2 stimulated processing of several receptors with known functions in endothelial cell biology.
CONCLUSIONS:These results provide the first evidence for a role for ADAM17 in pathological neovascularization in vivo. Because ADAM17 does not appear to be required for normal developmental angiogenesis or vascular homeostasis, it could emerge as a good target for treatment of pathological neovascularization. |
| doi_str_mv | 10.1161/CIRCRESAHA.109.207415 |
| format | Article |
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OBJECTIVE:The objective of this study was to inactivate ADAM17 in endothelial cells or in pericytes to determine how this affects developmental angiogenesis, pathological retinal neovascularization and heterotopic tumor growth.
METHODS AND RESULTS:We generated animals in which floxed ADAM17 was removed by Tie2-Cre in endothelial cells, or by smooth muscle (sm) Cre in smooth muscle cells and pericytes. There were no evident developmental defects in either conditional knockout strain, but pathological retinal neovascularization and growth of heterotopically injected tumor cells was reduced in Adam17flox/flox/Tie2-Cre mice, although not in Adam17flox/flox/sm-Cre mice. Moreover, lack of ADAM17 in endothelial cells decreased ex vivo chord formation, and this could be largely restored by addition of the ADAM17 substrate HB-EGF (heparin-binding epidermal growth factor-like growth factor). Finally we found that ADAM17 is important for the VEGF receptor 2 stimulated processing of several receptors with known functions in endothelial cell biology.
CONCLUSIONS:These results provide the first evidence for a role for ADAM17 in pathological neovascularization in vivo. Because ADAM17 does not appear to be required for normal developmental angiogenesis or vascular homeostasis, it could emerge as a good target for treatment of pathological neovascularization.</description><identifier>ISSN: 0009-7330</identifier><identifier>EISSN: 1524-4571</identifier><identifier>DOI: 10.1161/CIRCRESAHA.109.207415</identifier><identifier>PMID: 20110534</identifier><identifier>CODEN: CIRUAL</identifier><language>eng</language><publisher>Hagerstown, MD: American Heart Association, Inc</publisher><subject>Actins - metabolism ; ADAM Proteins - deficiency ; ADAM Proteins - genetics ; ADAM17 Protein ; Animals ; Biological and medical sciences ; Cell Movement ; Cell Proliferation ; Cells, Cultured ; Disease Models, Animal ; Endothelial Cells - enzymology ; Fundamental and applied biological sciences. Psychology ; Heparin-binding EGF-like Growth Factor ; Integrases - genetics ; Intercellular Signaling Peptides and Proteins - metabolism ; Medical sciences ; Melanoma, Experimental - blood supply ; Melanoma, Experimental - pathology ; Melanoma, Experimental - prevention & control ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Neovascularization, Pathologic - enzymology ; Neovascularization, Pathologic - genetics ; Neovascularization, Pathologic - prevention & control ; Ophthalmology ; Pericytes - enzymology ; Promoter Regions, Genetic ; Receptor Protein-Tyrosine Kinases - genetics ; Receptor, TIE-2 ; Retinal Neovascularization - enzymology ; Retinal Neovascularization - genetics ; Retinal Neovascularization - prevention & control ; Retinopathies ; Swine ; Time Factors ; Tumor Burden ; Vascular Endothelial Growth Factor A - metabolism ; Vascular Endothelial Growth Factor Receptor-2 - metabolism ; Vertebrates: cardiovascular system</subject><ispartof>Circulation research, 2010-03, Vol.106 (5), p.932-940</ispartof><rights>2010 American Heart Association, Inc.</rights><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4854-6453cff527b961636922fd78e9afc7d76ee6bf121cb8d2e1ea15982ad801df9f3</citedby><cites>FETCH-LOGICAL-c4854-6453cff527b961636922fd78e9afc7d76ee6bf121cb8d2e1ea15982ad801df9f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,3687,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=22607323$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20110534$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Weskamp, Gisela</creatorcontrib><creatorcontrib>Mendelson, Karen</creatorcontrib><creatorcontrib>Swendeman, Steve</creatorcontrib><creatorcontrib>Le Gall, Sylvain</creatorcontrib><creatorcontrib>Ma, Yan</creatorcontrib><creatorcontrib>Lyman, Stephen</creatorcontrib><creatorcontrib>Hinoki, Akinari</creatorcontrib><creatorcontrib>Eguchi, Satoru</creatorcontrib><creatorcontrib>Guaiquil, Victor</creatorcontrib><creatorcontrib>Horiuchi, Keisuke</creatorcontrib><creatorcontrib>Blobel, Carl P</creatorcontrib><title>Pathological Neovascularization Is Reduced by Inactivation of ADAM17 in Endothelial Cells but Not in Pericytes</title><title>Circulation research</title><addtitle>Circ Res</addtitle><description>RATIONALE:Pathological neovascularization is a critical component of diseases such as proliferative retinopathies, cancer and rheumatoid arthritis, yet much remains to be learned about the underlying causes. Previous studies showed that vascular endothelial growth factor (VEGF)-A activates the membrane-anchored metalloproteinase ADAM17 (a disintegrin and metalloproteinase 17) in endothelial cells, thereby stimulating crosstalk between VEGF receptor 2 and extracellular signal-regulated kinase. These findings raised interesting questions about the role of ADAM17 in angiogenesis and neovascularization in vivo.
OBJECTIVE:The objective of this study was to inactivate ADAM17 in endothelial cells or in pericytes to determine how this affects developmental angiogenesis, pathological retinal neovascularization and heterotopic tumor growth.
METHODS AND RESULTS:We generated animals in which floxed ADAM17 was removed by Tie2-Cre in endothelial cells, or by smooth muscle (sm) Cre in smooth muscle cells and pericytes. There were no evident developmental defects in either conditional knockout strain, but pathological retinal neovascularization and growth of heterotopically injected tumor cells was reduced in Adam17flox/flox/Tie2-Cre mice, although not in Adam17flox/flox/sm-Cre mice. Moreover, lack of ADAM17 in endothelial cells decreased ex vivo chord formation, and this could be largely restored by addition of the ADAM17 substrate HB-EGF (heparin-binding epidermal growth factor-like growth factor). Finally we found that ADAM17 is important for the VEGF receptor 2 stimulated processing of several receptors with known functions in endothelial cell biology.
CONCLUSIONS:These results provide the first evidence for a role for ADAM17 in pathological neovascularization in vivo. Because ADAM17 does not appear to be required for normal developmental angiogenesis or vascular homeostasis, it could emerge as a good target for treatment of pathological neovascularization.</description><subject>Actins - metabolism</subject><subject>ADAM Proteins - deficiency</subject><subject>ADAM Proteins - genetics</subject><subject>ADAM17 Protein</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cell Movement</subject><subject>Cell Proliferation</subject><subject>Cells, Cultured</subject><subject>Disease Models, Animal</subject><subject>Endothelial Cells - enzymology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Heparin-binding EGF-like Growth Factor</subject><subject>Integrases - genetics</subject><subject>Intercellular Signaling Peptides and Proteins - metabolism</subject><subject>Medical sciences</subject><subject>Melanoma, Experimental - blood supply</subject><subject>Melanoma, Experimental - pathology</subject><subject>Melanoma, Experimental - prevention & control</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Neovascularization, Pathologic - enzymology</subject><subject>Neovascularization, Pathologic - genetics</subject><subject>Neovascularization, Pathologic - prevention & control</subject><subject>Ophthalmology</subject><subject>Pericytes - enzymology</subject><subject>Promoter Regions, Genetic</subject><subject>Receptor Protein-Tyrosine Kinases - genetics</subject><subject>Receptor, TIE-2</subject><subject>Retinal Neovascularization - enzymology</subject><subject>Retinal Neovascularization - genetics</subject><subject>Retinal Neovascularization - prevention & control</subject><subject>Retinopathies</subject><subject>Swine</subject><subject>Time Factors</subject><subject>Tumor Burden</subject><subject>Vascular Endothelial Growth Factor A - metabolism</subject><subject>Vascular Endothelial Growth Factor Receptor-2 - metabolism</subject><subject>Vertebrates: cardiovascular system</subject><issn>0009-7330</issn><issn>1524-4571</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVklFv0zAUhSMEYt3gJ4DygnhK8XWcOHlBqkphlcaYCjxbjnO9Gtx42E6n7tfjkbLBky2f755r-9wsewVkDlDDu-V6s9ysvi7OF3Mg7ZwSzqB6ks2goqxgFYen2YwQ0ha8LMlJdhrCD0KAlbR9np1QAkCqks2y4UrGrbPu2ihp80t0exnUaKU3dzIaN-TrkG-wHxX2eXfI14NU0ewnyel88WHxGXhuhnw19C5u0Zpks0RrQ96NMb908V68Qm_UIWJ4kT3T0gZ8eVzPsu8fV9-W58XFl0_r5eKiUKypWFGzqlRaV5R3bQ11WbeU6p432EqteM9rxLrTQEF1TU8RUELVNlT2DYFet7o8y95Pvjdjt8Ne4RC9tOLGm530B-GkEf8rg9mKa7cXtGGUsSYZvD0aePdrxBDFzgSV3iUHdGMQ6Vd5w5umSmQ1kcq7EDzqhy5AxH1U4jGqdNSKKapU9_rfKz5U_c0mAW-OQIpEWu3loEx45GhNeEnLxLGJu3U2og8_7XiLXmxR2rgVaQZISYAWyTftoCUF-TMIvwGOtK5I</recordid><startdate>20100319</startdate><enddate>20100319</enddate><creator>Weskamp, Gisela</creator><creator>Mendelson, Karen</creator><creator>Swendeman, Steve</creator><creator>Le Gall, Sylvain</creator><creator>Ma, Yan</creator><creator>Lyman, Stephen</creator><creator>Hinoki, Akinari</creator><creator>Eguchi, Satoru</creator><creator>Guaiquil, Victor</creator><creator>Horiuchi, Keisuke</creator><creator>Blobel, Carl P</creator><general>American Heart Association, Inc</general><general>Lippincott Williams & Wilkins</general><scope>IQODW</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>7X8</scope><scope>5PM</scope></search><sort><creationdate>20100319</creationdate><title>Pathological Neovascularization Is Reduced by Inactivation of ADAM17 in Endothelial Cells but Not in Pericytes</title><author>Weskamp, Gisela ; Mendelson, Karen ; Swendeman, Steve ; Le Gall, Sylvain ; Ma, Yan ; Lyman, Stephen ; Hinoki, Akinari ; Eguchi, Satoru ; Guaiquil, Victor ; Horiuchi, Keisuke ; Blobel, Carl P</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4854-6453cff527b961636922fd78e9afc7d76ee6bf121cb8d2e1ea15982ad801df9f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Actins - metabolism</topic><topic>ADAM Proteins - deficiency</topic><topic>ADAM Proteins - genetics</topic><topic>ADAM17 Protein</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cell Movement</topic><topic>Cell Proliferation</topic><topic>Cells, Cultured</topic><topic>Disease Models, Animal</topic><topic>Endothelial Cells - enzymology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Heparin-binding EGF-like Growth Factor</topic><topic>Integrases - genetics</topic><topic>Intercellular Signaling Peptides and Proteins - metabolism</topic><topic>Medical sciences</topic><topic>Melanoma, Experimental - blood supply</topic><topic>Melanoma, Experimental - pathology</topic><topic>Melanoma, Experimental - prevention & control</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Neovascularization, Pathologic - enzymology</topic><topic>Neovascularization, Pathologic - genetics</topic><topic>Neovascularization, Pathologic - prevention & control</topic><topic>Ophthalmology</topic><topic>Pericytes - enzymology</topic><topic>Promoter Regions, Genetic</topic><topic>Receptor Protein-Tyrosine Kinases - genetics</topic><topic>Receptor, TIE-2</topic><topic>Retinal Neovascularization - enzymology</topic><topic>Retinal Neovascularization - genetics</topic><topic>Retinal Neovascularization - prevention & control</topic><topic>Retinopathies</topic><topic>Swine</topic><topic>Time Factors</topic><topic>Tumor Burden</topic><topic>Vascular Endothelial Growth Factor A - metabolism</topic><topic>Vascular Endothelial Growth Factor Receptor-2 - metabolism</topic><topic>Vertebrates: cardiovascular system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Weskamp, Gisela</creatorcontrib><creatorcontrib>Mendelson, Karen</creatorcontrib><creatorcontrib>Swendeman, Steve</creatorcontrib><creatorcontrib>Le Gall, Sylvain</creatorcontrib><creatorcontrib>Ma, Yan</creatorcontrib><creatorcontrib>Lyman, Stephen</creatorcontrib><creatorcontrib>Hinoki, Akinari</creatorcontrib><creatorcontrib>Eguchi, Satoru</creatorcontrib><creatorcontrib>Guaiquil, Victor</creatorcontrib><creatorcontrib>Horiuchi, Keisuke</creatorcontrib><creatorcontrib>Blobel, Carl P</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Circulation research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Weskamp, Gisela</au><au>Mendelson, Karen</au><au>Swendeman, Steve</au><au>Le Gall, Sylvain</au><au>Ma, Yan</au><au>Lyman, Stephen</au><au>Hinoki, Akinari</au><au>Eguchi, Satoru</au><au>Guaiquil, Victor</au><au>Horiuchi, Keisuke</au><au>Blobel, Carl P</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Pathological Neovascularization Is Reduced by Inactivation of ADAM17 in Endothelial Cells but Not in Pericytes</atitle><jtitle>Circulation research</jtitle><addtitle>Circ Res</addtitle><date>2010-03-19</date><risdate>2010</risdate><volume>106</volume><issue>5</issue><spage>932</spage><epage>940</epage><pages>932-940</pages><issn>0009-7330</issn><eissn>1524-4571</eissn><coden>CIRUAL</coden><abstract>RATIONALE:Pathological neovascularization is a critical component of diseases such as proliferative retinopathies, cancer and rheumatoid arthritis, yet much remains to be learned about the underlying causes. Previous studies showed that vascular endothelial growth factor (VEGF)-A activates the membrane-anchored metalloproteinase ADAM17 (a disintegrin and metalloproteinase 17) in endothelial cells, thereby stimulating crosstalk between VEGF receptor 2 and extracellular signal-regulated kinase. These findings raised interesting questions about the role of ADAM17 in angiogenesis and neovascularization in vivo.
OBJECTIVE:The objective of this study was to inactivate ADAM17 in endothelial cells or in pericytes to determine how this affects developmental angiogenesis, pathological retinal neovascularization and heterotopic tumor growth.
METHODS AND RESULTS:We generated animals in which floxed ADAM17 was removed by Tie2-Cre in endothelial cells, or by smooth muscle (sm) Cre in smooth muscle cells and pericytes. There were no evident developmental defects in either conditional knockout strain, but pathological retinal neovascularization and growth of heterotopically injected tumor cells was reduced in Adam17flox/flox/Tie2-Cre mice, although not in Adam17flox/flox/sm-Cre mice. Moreover, lack of ADAM17 in endothelial cells decreased ex vivo chord formation, and this could be largely restored by addition of the ADAM17 substrate HB-EGF (heparin-binding epidermal growth factor-like growth factor). Finally we found that ADAM17 is important for the VEGF receptor 2 stimulated processing of several receptors with known functions in endothelial cell biology.
CONCLUSIONS:These results provide the first evidence for a role for ADAM17 in pathological neovascularization in vivo. Because ADAM17 does not appear to be required for normal developmental angiogenesis or vascular homeostasis, it could emerge as a good target for treatment of pathological neovascularization.</abstract><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>20110534</pmid><doi>10.1161/CIRCRESAHA.109.207415</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Actins - metabolism ADAM Proteins - deficiency ADAM Proteins - genetics ADAM17 Protein Animals Biological and medical sciences Cell Movement Cell Proliferation Cells, Cultured Disease Models, Animal Endothelial Cells - enzymology Fundamental and applied biological sciences. Psychology Heparin-binding EGF-like Growth Factor Integrases - genetics Intercellular Signaling Peptides and Proteins - metabolism Medical sciences Melanoma, Experimental - blood supply Melanoma, Experimental - pathology Melanoma, Experimental - prevention & control Mice Mice, Inbred C57BL Mice, Knockout Neovascularization, Pathologic - enzymology Neovascularization, Pathologic - genetics Neovascularization, Pathologic - prevention & control Ophthalmology Pericytes - enzymology Promoter Regions, Genetic Receptor Protein-Tyrosine Kinases - genetics Receptor, TIE-2 Retinal Neovascularization - enzymology Retinal Neovascularization - genetics Retinal Neovascularization - prevention & control Retinopathies Swine Time Factors Tumor Burden Vascular Endothelial Growth Factor A - metabolism Vascular Endothelial Growth Factor Receptor-2 - metabolism Vertebrates: cardiovascular system |
| title | Pathological Neovascularization Is Reduced by Inactivation of ADAM17 in Endothelial Cells but Not in Pericytes |
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