Sustained Placental Growth Factor-2 Treatment Does Not Aggravate Advanced Atherosclerosis in Ischemic Cardiomyopathy
Angiogenic growth factor therapy for ischemic cardiovascular disease carries a risk of stimulating atherosclerotic plaque growth. We evaluated risk benefit ratio of sustained administration of recombinant human placental growth factor (rhPlGF)-2 in mice with advanced atherosclerosis and chronic isch...
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| Veröffentlicht in: | Journal of cardiovascular translational research 2017-08, Vol.10 (4), p.348-358 |
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| creator | Wu, Ming Pokreisz, Peter Swinnen, Melissa Caluwe, Ellen Gillijns, Hilde Vanden Driessche, Nina Casazza, Andrea Verbeken, Erik Collen, Desire Janssens, Stefan |
| description | Angiogenic growth factor therapy for ischemic cardiovascular disease carries a risk of stimulating atherosclerotic plaque growth. We evaluated risk benefit ratio of sustained administration of recombinant human placental growth factor (rhPlGF)-2 in mice with advanced atherosclerosis and chronic ischemic cardiomyopathy. We maintained apolipoprotein E-deficient mice on a high cholesterol diet and induced myocardial infarction by transient ligation at 4 weeks. At 8 weeks, we assessed left ventricular (LV) function and randomized mice to receive rhPlGF-2 or vehicle (VEH) subcutaneously for 28 days. Administration of rhPlGF-2 significantly increased PlGF plasma levels without adverse hemodynamic or systemic inflammatory effects. RhPlGF-2 did not increase plaque area, composition, or vulnerability in the aortic arch. RhPlGF-2 significantly improved contractile function and reduced LV end-systolic and end-diastolic volume indices with a concomitant increase in capillary and arteriolar density in ischemic myocardium. RhPlGF-2 may represent a promising therapeutic strategy in chronic ischemic cardiomyopathy. |
| doi_str_mv | 10.1007/s12265-017-9742-4 |
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We evaluated risk benefit ratio of sustained administration of recombinant human placental growth factor (rhPlGF)-2 in mice with advanced atherosclerosis and chronic ischemic cardiomyopathy. We maintained apolipoprotein E-deficient mice on a high cholesterol diet and induced myocardial infarction by transient ligation at 4 weeks. At 8 weeks, we assessed left ventricular (LV) function and randomized mice to receive rhPlGF-2 or vehicle (VEH) subcutaneously for 28 days. Administration of rhPlGF-2 significantly increased PlGF plasma levels without adverse hemodynamic or systemic inflammatory effects. RhPlGF-2 did not increase plaque area, composition, or vulnerability in the aortic arch. RhPlGF-2 significantly improved contractile function and reduced LV end-systolic and end-diastolic volume indices with a concomitant increase in capillary and arteriolar density in ischemic myocardium. RhPlGF-2 may represent a promising therapeutic strategy in chronic ischemic cardiomyopathy.</description><identifier>ISSN: 1937-5387</identifier><identifier>EISSN: 1937-5395</identifier><identifier>DOI: 10.1007/s12265-017-9742-4</identifier><identifier>PMID: 28397162</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Angiogenesis Inducing Agents - administration & dosage ; Angiogenesis Inducing Agents - toxicity ; Animals ; Aorta - drug effects ; Aorta - pathology ; Aorta - physiopathology ; Aortic Diseases - drug therapy ; Aortic Diseases - pathology ; Aortic Diseases - physiopathology ; Atherosclerosis - drug therapy ; Atherosclerosis - pathology ; Atherosclerosis - physiopathology ; Biomedical Engineering and Bioengineering ; Biomedicine ; Cardiology ; Cardiomyopathies - diagnostic imaging ; Cardiomyopathies - drug therapy ; Cardiomyopathies - physiopathology ; Cholesterol, Dietary ; Chronic Disease ; Disease Models, Animal ; Human Genetics ; Infusions, Subcutaneous ; Male ; Medicine ; Medicine & Public Health ; Mice, Knockout, ApoE ; Myocardial Contraction - drug effects ; Myocardial Infarction - diagnostic imaging ; Myocardial Infarction - drug therapy ; Myocardial Infarction - physiopathology ; Neovascularization, Physiologic - drug effects ; Original Article ; Placenta Growth Factor - administration & dosage ; Placenta Growth Factor - toxicity ; Plaque, Atherosclerotic ; Recombinant Proteins - administration & dosage ; Recovery of Function ; Stroke Volume - drug effects ; Time Factors ; Vascular Stiffness - drug effects ; Ventricular Function, Left - drug effects ; Ventricular Remodeling - drug effects</subject><ispartof>Journal of cardiovascular translational research, 2017-08, Vol.10 (4), p.348-358</ispartof><rights>Springer Science+Business Media New York 2017</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c344t-41b4a8c31942eb4d69eb5ec89f6a209a26020e77ef0ca9ee5da59d319de22cec3</citedby><cites>FETCH-LOGICAL-c344t-41b4a8c31942eb4d69eb5ec89f6a209a26020e77ef0ca9ee5da59d319de22cec3</cites><orcidid>0000-0003-2810-9000</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12265-017-9742-4$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12265-017-9742-4$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27922,27923,41486,42555,51317</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28397162$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wu, Ming</creatorcontrib><creatorcontrib>Pokreisz, Peter</creatorcontrib><creatorcontrib>Swinnen, Melissa</creatorcontrib><creatorcontrib>Caluwe, Ellen</creatorcontrib><creatorcontrib>Gillijns, Hilde</creatorcontrib><creatorcontrib>Vanden Driessche, Nina</creatorcontrib><creatorcontrib>Casazza, Andrea</creatorcontrib><creatorcontrib>Verbeken, Erik</creatorcontrib><creatorcontrib>Collen, Desire</creatorcontrib><creatorcontrib>Janssens, Stefan</creatorcontrib><title>Sustained Placental Growth Factor-2 Treatment Does Not Aggravate Advanced Atherosclerosis in Ischemic Cardiomyopathy</title><title>Journal of cardiovascular translational research</title><addtitle>J. of Cardiovasc. Trans. Res</addtitle><addtitle>J Cardiovasc Transl Res</addtitle><description>Angiogenic growth factor therapy for ischemic cardiovascular disease carries a risk of stimulating atherosclerotic plaque growth. We evaluated risk benefit ratio of sustained administration of recombinant human placental growth factor (rhPlGF)-2 in mice with advanced atherosclerosis and chronic ischemic cardiomyopathy. We maintained apolipoprotein E-deficient mice on a high cholesterol diet and induced myocardial infarction by transient ligation at 4 weeks. At 8 weeks, we assessed left ventricular (LV) function and randomized mice to receive rhPlGF-2 or vehicle (VEH) subcutaneously for 28 days. Administration of rhPlGF-2 significantly increased PlGF plasma levels without adverse hemodynamic or systemic inflammatory effects. RhPlGF-2 did not increase plaque area, composition, or vulnerability in the aortic arch. RhPlGF-2 significantly improved contractile function and reduced LV end-systolic and end-diastolic volume indices with a concomitant increase in capillary and arteriolar density in ischemic myocardium. RhPlGF-2 may represent a promising therapeutic strategy in chronic ischemic cardiomyopathy.</description><subject>Angiogenesis Inducing Agents - administration & dosage</subject><subject>Angiogenesis Inducing Agents - toxicity</subject><subject>Animals</subject><subject>Aorta - drug effects</subject><subject>Aorta - pathology</subject><subject>Aorta - physiopathology</subject><subject>Aortic Diseases - drug therapy</subject><subject>Aortic Diseases - pathology</subject><subject>Aortic Diseases - physiopathology</subject><subject>Atherosclerosis - drug therapy</subject><subject>Atherosclerosis - pathology</subject><subject>Atherosclerosis - physiopathology</subject><subject>Biomedical Engineering and Bioengineering</subject><subject>Biomedicine</subject><subject>Cardiology</subject><subject>Cardiomyopathies - diagnostic imaging</subject><subject>Cardiomyopathies - drug therapy</subject><subject>Cardiomyopathies - physiopathology</subject><subject>Cholesterol, Dietary</subject><subject>Chronic Disease</subject><subject>Disease Models, Animal</subject><subject>Human Genetics</subject><subject>Infusions, Subcutaneous</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mice, Knockout, ApoE</subject><subject>Myocardial Contraction - drug effects</subject><subject>Myocardial Infarction - diagnostic imaging</subject><subject>Myocardial Infarction - drug therapy</subject><subject>Myocardial Infarction - physiopathology</subject><subject>Neovascularization, Physiologic - drug effects</subject><subject>Original Article</subject><subject>Placenta Growth Factor - administration & dosage</subject><subject>Placenta Growth Factor - toxicity</subject><subject>Plaque, Atherosclerotic</subject><subject>Recombinant Proteins - administration & dosage</subject><subject>Recovery of Function</subject><subject>Stroke Volume - drug effects</subject><subject>Time Factors</subject><subject>Vascular Stiffness - drug effects</subject><subject>Ventricular Function, Left - drug effects</subject><subject>Ventricular Remodeling - drug effects</subject><issn>1937-5387</issn><issn>1937-5395</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kMtOwzAQRS0E4lH4ADbISzYB23HieFmVp4QAibK2ps60DUriYjtF_XtcFViysS3NuVfjQ8g5Z1ecMXUduBBlkTGuMq2kyOQeOeY6V1mR62L_712pI3ISwgdjpWBKHZIjUeVa8VIck_g2hAhNjzV9bcFiH6Gl9959xSW9AxudzwSdeoTYpRm9cRjos4t0vFh4WENEOq7X0NuUH8clehdsuz2bQJuePga7xK6xdAK-bly3cSuIy80pOZhDG_Ds5x6R97vb6eQhe3q5f5yMnzKbSxkzyWcSKptzLQXOZF1qnBVoKz0vQTANomSCoVI4ZxY0YlFDoeuE1yiERZuPyOWud-Xd54Ahmq4JFtsWenRDMLyqSlXkhVIJ5TvUpuWDx7lZ-aYDvzGcma1ss5NtkmyzlW1kylz81A-zDuu_xK_dBIgdENKoX6A3H27wffryP63fVPyMJg</recordid><startdate>20170801</startdate><enddate>20170801</enddate><creator>Wu, Ming</creator><creator>Pokreisz, Peter</creator><creator>Swinnen, Melissa</creator><creator>Caluwe, Ellen</creator><creator>Gillijns, Hilde</creator><creator>Vanden Driessche, Nina</creator><creator>Casazza, Andrea</creator><creator>Verbeken, Erik</creator><creator>Collen, Desire</creator><creator>Janssens, Stefan</creator><general>Springer US</general><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><orcidid>https://orcid.org/0000-0003-2810-9000</orcidid></search><sort><creationdate>20170801</creationdate><title>Sustained Placental Growth Factor-2 Treatment Does Not Aggravate Advanced Atherosclerosis in Ischemic Cardiomyopathy</title><author>Wu, Ming ; Pokreisz, Peter ; Swinnen, Melissa ; Caluwe, Ellen ; Gillijns, Hilde ; Vanden Driessche, Nina ; Casazza, Andrea ; Verbeken, Erik ; Collen, Desire ; Janssens, Stefan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c344t-41b4a8c31942eb4d69eb5ec89f6a209a26020e77ef0ca9ee5da59d319de22cec3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Angiogenesis Inducing Agents - administration & dosage</topic><topic>Angiogenesis Inducing Agents - toxicity</topic><topic>Animals</topic><topic>Aorta - drug effects</topic><topic>Aorta - pathology</topic><topic>Aorta - physiopathology</topic><topic>Aortic Diseases - drug therapy</topic><topic>Aortic Diseases - pathology</topic><topic>Aortic Diseases - physiopathology</topic><topic>Atherosclerosis - drug therapy</topic><topic>Atherosclerosis - pathology</topic><topic>Atherosclerosis - physiopathology</topic><topic>Biomedical Engineering and Bioengineering</topic><topic>Biomedicine</topic><topic>Cardiology</topic><topic>Cardiomyopathies - diagnostic imaging</topic><topic>Cardiomyopathies - drug therapy</topic><topic>Cardiomyopathies - physiopathology</topic><topic>Cholesterol, Dietary</topic><topic>Chronic Disease</topic><topic>Disease Models, Animal</topic><topic>Human Genetics</topic><topic>Infusions, Subcutaneous</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Mice, Knockout, ApoE</topic><topic>Myocardial Contraction - drug effects</topic><topic>Myocardial Infarction - diagnostic imaging</topic><topic>Myocardial Infarction - drug therapy</topic><topic>Myocardial Infarction - physiopathology</topic><topic>Neovascularization, Physiologic - drug effects</topic><topic>Original Article</topic><topic>Placenta Growth Factor - administration & dosage</topic><topic>Placenta Growth Factor - toxicity</topic><topic>Plaque, Atherosclerotic</topic><topic>Recombinant Proteins - administration & dosage</topic><topic>Recovery of Function</topic><topic>Stroke Volume - drug effects</topic><topic>Time Factors</topic><topic>Vascular Stiffness - drug effects</topic><topic>Ventricular Function, Left - drug effects</topic><topic>Ventricular Remodeling - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wu, Ming</creatorcontrib><creatorcontrib>Pokreisz, Peter</creatorcontrib><creatorcontrib>Swinnen, Melissa</creatorcontrib><creatorcontrib>Caluwe, Ellen</creatorcontrib><creatorcontrib>Gillijns, Hilde</creatorcontrib><creatorcontrib>Vanden Driessche, Nina</creatorcontrib><creatorcontrib>Casazza, Andrea</creatorcontrib><creatorcontrib>Verbeken, Erik</creatorcontrib><creatorcontrib>Collen, Desire</creatorcontrib><creatorcontrib>Janssens, Stefan</creatorcontrib><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>Journal of cardiovascular translational research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wu, Ming</au><au>Pokreisz, Peter</au><au>Swinnen, Melissa</au><au>Caluwe, Ellen</au><au>Gillijns, Hilde</au><au>Vanden Driessche, Nina</au><au>Casazza, Andrea</au><au>Verbeken, Erik</au><au>Collen, Desire</au><au>Janssens, Stefan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sustained Placental Growth Factor-2 Treatment Does Not Aggravate Advanced Atherosclerosis in Ischemic Cardiomyopathy</atitle><jtitle>Journal of cardiovascular translational research</jtitle><stitle>J. of Cardiovasc. Trans. Res</stitle><addtitle>J Cardiovasc Transl Res</addtitle><date>2017-08-01</date><risdate>2017</risdate><volume>10</volume><issue>4</issue><spage>348</spage><epage>358</epage><pages>348-358</pages><issn>1937-5387</issn><eissn>1937-5395</eissn><abstract>Angiogenic growth factor therapy for ischemic cardiovascular disease carries a risk of stimulating atherosclerotic plaque growth. We evaluated risk benefit ratio of sustained administration of recombinant human placental growth factor (rhPlGF)-2 in mice with advanced atherosclerosis and chronic ischemic cardiomyopathy. We maintained apolipoprotein E-deficient mice on a high cholesterol diet and induced myocardial infarction by transient ligation at 4 weeks. At 8 weeks, we assessed left ventricular (LV) function and randomized mice to receive rhPlGF-2 or vehicle (VEH) subcutaneously for 28 days. Administration of rhPlGF-2 significantly increased PlGF plasma levels without adverse hemodynamic or systemic inflammatory effects. RhPlGF-2 did not increase plaque area, composition, or vulnerability in the aortic arch. RhPlGF-2 significantly improved contractile function and reduced LV end-systolic and end-diastolic volume indices with a concomitant increase in capillary and arteriolar density in ischemic myocardium. RhPlGF-2 may represent a promising therapeutic strategy in chronic ischemic cardiomyopathy.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>28397162</pmid><doi>10.1007/s12265-017-9742-4</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0003-2810-9000</orcidid></addata></record> |
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| ispartof | Journal of cardiovascular translational research, 2017-08, Vol.10 (4), p.348-358 |
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| subjects | Angiogenesis Inducing Agents - administration & dosage Angiogenesis Inducing Agents - toxicity Animals Aorta - drug effects Aorta - pathology Aorta - physiopathology Aortic Diseases - drug therapy Aortic Diseases - pathology Aortic Diseases - physiopathology Atherosclerosis - drug therapy Atherosclerosis - pathology Atherosclerosis - physiopathology Biomedical Engineering and Bioengineering Biomedicine Cardiology Cardiomyopathies - diagnostic imaging Cardiomyopathies - drug therapy Cardiomyopathies - physiopathology Cholesterol, Dietary Chronic Disease Disease Models, Animal Human Genetics Infusions, Subcutaneous Male Medicine Medicine & Public Health Mice, Knockout, ApoE Myocardial Contraction - drug effects Myocardial Infarction - diagnostic imaging Myocardial Infarction - drug therapy Myocardial Infarction - physiopathology Neovascularization, Physiologic - drug effects Original Article Placenta Growth Factor - administration & dosage Placenta Growth Factor - toxicity Plaque, Atherosclerotic Recombinant Proteins - administration & dosage Recovery of Function Stroke Volume - drug effects Time Factors Vascular Stiffness - drug effects Ventricular Function, Left - drug effects Ventricular Remodeling - drug effects |
| title | Sustained Placental Growth Factor-2 Treatment Does Not Aggravate Advanced Atherosclerosis in Ischemic Cardiomyopathy |
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