Osteopontin expression and adventitial angiogenesis induced by local vascular endothelial growth factor 165 reduces experimental aortic calcification
Vascular calcification is a common pathologic and precisely regulated process involving bone-associated proteins such as osteopontin. In this study, we investigated mechanisms by which recombinant human vascular endothelial growth factor 165 protects the arterial wall from severe vascular remodeling...
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| Veröffentlicht in: | The Journal of thoracic and cardiovascular surgery 2005-04, Vol.129 (4), p.773-781 |
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| creator | Seipelt, Ralf G. Backer, Carl L. Mavroudis, Constantine Stellmach, Veronica Cornwell, Mona Seipelt, Ingrid M. Schoendube, Friedrich A. Crawford, Susan E. |
| description | Vascular calcification is a common pathologic and precisely regulated process involving bone-associated proteins such as osteopontin. In this study, we investigated mechanisms by which recombinant human vascular endothelial growth factor 165 protects the arterial wall from severe vascular remodeling, including calcification, a newly discovered biologic action of vascular endothelial growth factor.
In a rabbit model of thoracic aortic end-to-end anastomosis that simulates cardiovascular intervention, recombinant human vascular endothelial growth factor 165 at a dose of 0.75 μg (n = 19) or albumin (control; n = 19) was delivered intraluminally and on the serosal surface. Animals were killed, and aortic tissue was evaluated by Western blotting, immunohistochemistry, and immunofluorescence at 4, 8, and 24 hours; 1 week; and 1 month after surgery.
All controls revealed extensive aortic medial calcification at 1 month, whereas calcification was significantly reduced or absent with vascular endothelial growth factor treatment. Compared with controls, vascular endothelial growth factor treatment resulted in an earlier infiltration of macrophages in the vessel media (at 8 hours: 5.7 ± 2.3 macrophages per high-power field in control vs 32.1 ± 7.5 in vascular endothelial growth factor-treated aortas;
P < .001), whereas controls showed an increase in macrophages starting at 1 week (24.1 ± 6.9 vs 4.3 ± 1.8;
P < .001). Osteopontin expression was transiently increased and detected in macrophages and endothelial cells in vascular endothelial growth factor-treated vessels, and adventitial microvascular density was significantly increased by 1 week (9.5 ± 0.43 vs 25.0 ± 1.3;
P < .001).
Our data suggest that exogenous vascular endothelial growth factor is capable of increasing adventitial angiogenesis and shifting macrophage infiltration and osteopontin expression in the media to an earlier time point, thereby promoting prompt repair and diminishing vascular remodeling and calcification after acute vascular injury. |
| doi_str_mv | 10.1016/j.jtcvs.2004.06.039 |
| format | Article |
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In a rabbit model of thoracic aortic end-to-end anastomosis that simulates cardiovascular intervention, recombinant human vascular endothelial growth factor 165 at a dose of 0.75 μg (n = 19) or albumin (control; n = 19) was delivered intraluminally and on the serosal surface. Animals were killed, and aortic tissue was evaluated by Western blotting, immunohistochemistry, and immunofluorescence at 4, 8, and 24 hours; 1 week; and 1 month after surgery.
All controls revealed extensive aortic medial calcification at 1 month, whereas calcification was significantly reduced or absent with vascular endothelial growth factor treatment. Compared with controls, vascular endothelial growth factor treatment resulted in an earlier infiltration of macrophages in the vessel media (at 8 hours: 5.7 ± 2.3 macrophages per high-power field in control vs 32.1 ± 7.5 in vascular endothelial growth factor-treated aortas;
P < .001), whereas controls showed an increase in macrophages starting at 1 week (24.1 ± 6.9 vs 4.3 ± 1.8;
P < .001). Osteopontin expression was transiently increased and detected in macrophages and endothelial cells in vascular endothelial growth factor-treated vessels, and adventitial microvascular density was significantly increased by 1 week (9.5 ± 0.43 vs 25.0 ± 1.3;
P < .001).
Our data suggest that exogenous vascular endothelial growth factor is capable of increasing adventitial angiogenesis and shifting macrophage infiltration and osteopontin expression in the media to an earlier time point, thereby promoting prompt repair and diminishing vascular remodeling and calcification after acute vascular injury.</description><identifier>ISSN: 0022-5223</identifier><identifier>EISSN: 1097-685X</identifier><identifier>DOI: 10.1016/j.jtcvs.2004.06.039</identifier><identifier>PMID: 15821643</identifier><identifier>CODEN: JTCSAQ</identifier><language>eng</language><publisher>Philadelphia, PA: Mosby, Inc</publisher><subject>Animals ; Aorta, Thoracic - drug effects ; Aorta, Thoracic - pathology ; Aortic Diseases - prevention & control ; Biological and medical sciences ; Calcinosis - prevention & control ; Capillaries - drug effects ; Capillaries - pathology ; Disease Models, Animal ; Elastic Tissue - drug effects ; Elastic Tissue - pathology ; Endothelium, Vascular - drug effects ; Endothelium, Vascular - pathology ; Humans ; Macrophages - drug effects ; Macrophages - pathology ; Male ; Medical sciences ; Microcirculation - drug effects ; Microcirculation - pathology ; Neovascularization, Physiologic - drug effects ; Osteopontin ; Phosphoproteins - analysis ; Rabbits ; Sialoglycoproteins - analysis ; Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases ; Surgery of the heart ; Time Factors ; Tunica Media - drug effects ; Tunica Media - pathology ; Vascular Endothelial Growth Factor A - therapeutic use</subject><ispartof>The Journal of thoracic and cardiovascular surgery, 2005-04, Vol.129 (4), p.773-781</ispartof><rights>2005 The American Association for Thoracic Surgery</rights><rights>2005 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c464t-bd1c5026676ed971f0af117b0358a9df5c863fd50ced086345f24d9a5fbb07583</citedby><cites>FETCH-LOGICAL-c464t-bd1c5026676ed971f0af117b0358a9df5c863fd50ced086345f24d9a5fbb07583</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.jtcvs.2004.06.039$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16716461$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15821643$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Seipelt, Ralf G.</creatorcontrib><creatorcontrib>Backer, Carl L.</creatorcontrib><creatorcontrib>Mavroudis, Constantine</creatorcontrib><creatorcontrib>Stellmach, Veronica</creatorcontrib><creatorcontrib>Cornwell, Mona</creatorcontrib><creatorcontrib>Seipelt, Ingrid M.</creatorcontrib><creatorcontrib>Schoendube, Friedrich A.</creatorcontrib><creatorcontrib>Crawford, Susan E.</creatorcontrib><title>Osteopontin expression and adventitial angiogenesis induced by local vascular endothelial growth factor 165 reduces experimental aortic calcification</title><title>The Journal of thoracic and cardiovascular surgery</title><addtitle>J Thorac Cardiovasc Surg</addtitle><description>Vascular calcification is a common pathologic and precisely regulated process involving bone-associated proteins such as osteopontin. In this study, we investigated mechanisms by which recombinant human vascular endothelial growth factor 165 protects the arterial wall from severe vascular remodeling, including calcification, a newly discovered biologic action of vascular endothelial growth factor.
In a rabbit model of thoracic aortic end-to-end anastomosis that simulates cardiovascular intervention, recombinant human vascular endothelial growth factor 165 at a dose of 0.75 μg (n = 19) or albumin (control; n = 19) was delivered intraluminally and on the serosal surface. Animals were killed, and aortic tissue was evaluated by Western blotting, immunohistochemistry, and immunofluorescence at 4, 8, and 24 hours; 1 week; and 1 month after surgery.
All controls revealed extensive aortic medial calcification at 1 month, whereas calcification was significantly reduced or absent with vascular endothelial growth factor treatment. Compared with controls, vascular endothelial growth factor treatment resulted in an earlier infiltration of macrophages in the vessel media (at 8 hours: 5.7 ± 2.3 macrophages per high-power field in control vs 32.1 ± 7.5 in vascular endothelial growth factor-treated aortas;
P < .001), whereas controls showed an increase in macrophages starting at 1 week (24.1 ± 6.9 vs 4.3 ± 1.8;
P < .001). Osteopontin expression was transiently increased and detected in macrophages and endothelial cells in vascular endothelial growth factor-treated vessels, and adventitial microvascular density was significantly increased by 1 week (9.5 ± 0.43 vs 25.0 ± 1.3;
P < .001).
Our data suggest that exogenous vascular endothelial growth factor is capable of increasing adventitial angiogenesis and shifting macrophage infiltration and osteopontin expression in the media to an earlier time point, thereby promoting prompt repair and diminishing vascular remodeling and calcification after acute vascular injury.</description><subject>Animals</subject><subject>Aorta, Thoracic - drug effects</subject><subject>Aorta, Thoracic - pathology</subject><subject>Aortic Diseases - prevention & control</subject><subject>Biological and medical sciences</subject><subject>Calcinosis - prevention & control</subject><subject>Capillaries - drug effects</subject><subject>Capillaries - pathology</subject><subject>Disease Models, Animal</subject><subject>Elastic Tissue - drug effects</subject><subject>Elastic Tissue - pathology</subject><subject>Endothelium, Vascular - drug effects</subject><subject>Endothelium, Vascular - pathology</subject><subject>Humans</subject><subject>Macrophages - drug effects</subject><subject>Macrophages - pathology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Microcirculation - drug effects</subject><subject>Microcirculation - pathology</subject><subject>Neovascularization, Physiologic - drug effects</subject><subject>Osteopontin</subject><subject>Phosphoproteins - analysis</subject><subject>Rabbits</subject><subject>Sialoglycoproteins - analysis</subject><subject>Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases</subject><subject>Surgery of the heart</subject><subject>Time Factors</subject><subject>Tunica Media - drug effects</subject><subject>Tunica Media - pathology</subject><subject>Vascular Endothelial Growth Factor A - therapeutic use</subject><issn>0022-5223</issn><issn>1097-685X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kc1u1DAUhS0EotPCEyAhb6CrDNdJbCcLFlXFn1SpG5DYWY59PeNRJh5sZ0ofhPfFYUbqjpX_vnPu9bmEvGGwZsDEh916l80xrWuAdg1iDU3_jKwY9LISHf_5nKwA6rridd1ckMuUdgAggfUvyQXjXc1E26zIn_uUMRzClP1E8fchYko-TFRPlmp7xHKfvR7LeePDBidMPlE_2dmgpcMjHYMpr0edzDzqSHGyIW9xXCSbGB7yljptcoiUCU4jLrq01MHo98V8cQ4xe0OLjfHOG51L-VfkhdNjwtfn9Yr8-Pzp--3X6u7-y7fbm7vKtKLN1WCZ4VALIQXaXjIH2jEmB2h4p3vruOlE4yyH0iyUbctd3dpeczcMIHnXXJH3J99DDL9mTFntfTI4jnrCMCclpKwla9sCNifQxJBSRKcO5QM6PioGapmG2ql_01DLNBQIVaZRVG_P9vOwR_ukOcdfgHdnoASoRxf1ZHx64oQsmGCFuz5xW7_ZPviIKu31OBZbtpRNrO5Vq6RcHD-eSCyxHT1GlYzHqQRQVCYrG_x_W_4LR-67VQ</recordid><startdate>20050401</startdate><enddate>20050401</enddate><creator>Seipelt, Ralf G.</creator><creator>Backer, Carl L.</creator><creator>Mavroudis, Constantine</creator><creator>Stellmach, Veronica</creator><creator>Cornwell, Mona</creator><creator>Seipelt, Ingrid M.</creator><creator>Schoendube, Friedrich A.</creator><creator>Crawford, Susan E.</creator><general>Mosby, Inc</general><general>AATS/WTSA</general><general>Elsevier</general><scope>6I.</scope><scope>AAFTH</scope><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></search><sort><creationdate>20050401</creationdate><title>Osteopontin expression and adventitial angiogenesis induced by local vascular endothelial growth factor 165 reduces experimental aortic calcification</title><author>Seipelt, Ralf G. ; Backer, Carl L. ; Mavroudis, Constantine ; Stellmach, Veronica ; Cornwell, Mona ; Seipelt, Ingrid M. ; Schoendube, Friedrich A. ; Crawford, Susan E.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c464t-bd1c5026676ed971f0af117b0358a9df5c863fd50ced086345f24d9a5fbb07583</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>Aorta, Thoracic - drug effects</topic><topic>Aorta, Thoracic - pathology</topic><topic>Aortic Diseases - prevention & control</topic><topic>Biological and medical sciences</topic><topic>Calcinosis - prevention & control</topic><topic>Capillaries - drug effects</topic><topic>Capillaries - pathology</topic><topic>Disease Models, Animal</topic><topic>Elastic Tissue - drug effects</topic><topic>Elastic Tissue - pathology</topic><topic>Endothelium, Vascular - drug effects</topic><topic>Endothelium, Vascular - pathology</topic><topic>Humans</topic><topic>Macrophages - drug effects</topic><topic>Macrophages - pathology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Microcirculation - drug effects</topic><topic>Microcirculation - pathology</topic><topic>Neovascularization, Physiologic - drug effects</topic><topic>Osteopontin</topic><topic>Phosphoproteins - analysis</topic><topic>Rabbits</topic><topic>Sialoglycoproteins - analysis</topic><topic>Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases</topic><topic>Surgery of the heart</topic><topic>Time Factors</topic><topic>Tunica Media - drug effects</topic><topic>Tunica Media - pathology</topic><topic>Vascular Endothelial Growth Factor A - therapeutic use</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Seipelt, Ralf G.</creatorcontrib><creatorcontrib>Backer, Carl L.</creatorcontrib><creatorcontrib>Mavroudis, Constantine</creatorcontrib><creatorcontrib>Stellmach, Veronica</creatorcontrib><creatorcontrib>Cornwell, Mona</creatorcontrib><creatorcontrib>Seipelt, Ingrid M.</creatorcontrib><creatorcontrib>Schoendube, Friedrich A.</creatorcontrib><creatorcontrib>Crawford, Susan E.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><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><jtitle>The Journal of thoracic and cardiovascular surgery</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Seipelt, Ralf G.</au><au>Backer, Carl L.</au><au>Mavroudis, Constantine</au><au>Stellmach, Veronica</au><au>Cornwell, Mona</au><au>Seipelt, Ingrid M.</au><au>Schoendube, Friedrich A.</au><au>Crawford, Susan E.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Osteopontin expression and adventitial angiogenesis induced by local vascular endothelial growth factor 165 reduces experimental aortic calcification</atitle><jtitle>The Journal of thoracic and cardiovascular surgery</jtitle><addtitle>J Thorac Cardiovasc Surg</addtitle><date>2005-04-01</date><risdate>2005</risdate><volume>129</volume><issue>4</issue><spage>773</spage><epage>781</epage><pages>773-781</pages><issn>0022-5223</issn><eissn>1097-685X</eissn><coden>JTCSAQ</coden><abstract>Vascular calcification is a common pathologic and precisely regulated process involving bone-associated proteins such as osteopontin. In this study, we investigated mechanisms by which recombinant human vascular endothelial growth factor 165 protects the arterial wall from severe vascular remodeling, including calcification, a newly discovered biologic action of vascular endothelial growth factor.
In a rabbit model of thoracic aortic end-to-end anastomosis that simulates cardiovascular intervention, recombinant human vascular endothelial growth factor 165 at a dose of 0.75 μg (n = 19) or albumin (control; n = 19) was delivered intraluminally and on the serosal surface. Animals were killed, and aortic tissue was evaluated by Western blotting, immunohistochemistry, and immunofluorescence at 4, 8, and 24 hours; 1 week; and 1 month after surgery.
All controls revealed extensive aortic medial calcification at 1 month, whereas calcification was significantly reduced or absent with vascular endothelial growth factor treatment. Compared with controls, vascular endothelial growth factor treatment resulted in an earlier infiltration of macrophages in the vessel media (at 8 hours: 5.7 ± 2.3 macrophages per high-power field in control vs 32.1 ± 7.5 in vascular endothelial growth factor-treated aortas;
P < .001), whereas controls showed an increase in macrophages starting at 1 week (24.1 ± 6.9 vs 4.3 ± 1.8;
P < .001). Osteopontin expression was transiently increased and detected in macrophages and endothelial cells in vascular endothelial growth factor-treated vessels, and adventitial microvascular density was significantly increased by 1 week (9.5 ± 0.43 vs 25.0 ± 1.3;
P < .001).
Our data suggest that exogenous vascular endothelial growth factor is capable of increasing adventitial angiogenesis and shifting macrophage infiltration and osteopontin expression in the media to an earlier time point, thereby promoting prompt repair and diminishing vascular remodeling and calcification after acute vascular injury.</abstract><cop>Philadelphia, PA</cop><pub>Mosby, Inc</pub><pmid>15821643</pmid><doi>10.1016/j.jtcvs.2004.06.039</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Aorta, Thoracic - drug effects Aorta, Thoracic - pathology Aortic Diseases - prevention & control Biological and medical sciences Calcinosis - prevention & control Capillaries - drug effects Capillaries - pathology Disease Models, Animal Elastic Tissue - drug effects Elastic Tissue - pathology Endothelium, Vascular - drug effects Endothelium, Vascular - pathology Humans Macrophages - drug effects Macrophages - pathology Male Medical sciences Microcirculation - drug effects Microcirculation - pathology Neovascularization, Physiologic - drug effects Osteopontin Phosphoproteins - analysis Rabbits Sialoglycoproteins - analysis Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases Surgery of the heart Time Factors Tunica Media - drug effects Tunica Media - pathology Vascular Endothelial Growth Factor A - therapeutic use |
| title | Osteopontin expression and adventitial angiogenesis induced by local vascular endothelial growth factor 165 reduces experimental aortic calcification |
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