A murine model of deep vein thrombosis Characterization and validation in transgenic mice
Summary Deep vein thrombosis (DVT) occurs with high prevalence in association with a number of risk factors, including major surgery, trauma, obesity, bed rest (>5 days), cancer, a previous history of DVT, and several predisposing prothrombotic mutations. A novel murine model of DVT was developed...
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| Veröffentlicht in: | Thrombosis and haemostasis 2005-09, Vol.94 (3), p.498-503 |
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| creator | Cooley, Brian C. Szema, Linda Chen, Chao-Ying Schwab, Jeffrey P. Schmeling, Gregory |
| description | Summary
Deep vein thrombosis (DVT) occurs with high prevalence in association with a number of risk factors, including major surgery, trauma, obesity, bed rest (>5 days), cancer, a previous history of DVT, and several predisposing prothrombotic mutations. A novel murine model of DVT was developed for applications to preclinical studies of transgenically constructed prothrombotic lines and evaluation of new antithrombotic therapies. A transient direct-current electrical injury was induced in the common femoral vein of adult C57Bl/6 mice. A non-occlusive thrombus grew, peaking in size at 30 min, and regressing by 60 min, as revealed by histomorphometric volume reconstruction of the clot. Pre-heparinization greatly reduced clot formation at 10, 30, and 60 min (p |
| doi_str_mv | 10.1160/TH05-03-0170 |
| format | Article |
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Deep vein thrombosis (DVT) occurs with high prevalence in association with a number of risk factors, including major surgery, trauma, obesity, bed rest (>5 days), cancer, a previous history of DVT, and several predisposing prothrombotic mutations. A novel murine model of DVT was developed for applications to preclinical studies of transgenically constructed prothrombotic lines and evaluation of new antithrombotic therapies. A transient direct-current electrical injury was induced in the common femoral vein of adult C57Bl/6 mice. A non-occlusive thrombus grew, peaking in size at 30 min, and regressing by 60 min, as revealed by histomorphometric volume reconstruction of the clot. Pre-heparinization greatly reduced clot formation at 10, 30, and 60 min (p<0.01 versus non-heparinized). Homozygous FactorV Leiden mice (analogous to the clinical FactorV Leiden prothrombotic mutation) on a C57Bl/6 background had clot volumes more than twice those of wild-types at 30 min (0.121±0.018 mm
3
vs. 0.052±0.008 mm
3
, respectively; p<0.01). Scanning electron microscopy revealed a clot surface dominated by fibrin strands, in contrast to arterial thrombi which showed a platelet-dominated structure. This new model of DVT presents a quantifiable approach for evaluating thrombosis-related murine transgenic lines and for comparatively evaluating new pharmacologic approaches for prevention of DVT.</description><identifier>ISSN: 0340-6245</identifier><identifier>EISSN: 2567-689X</identifier><identifier>DOI: 10.1160/TH05-03-0170</identifier><identifier>PMID: 16268462</identifier><identifier>CODEN: THHADQ</identifier><language>eng</language><publisher>Stuttgart: Schattauer Verlag für Medizin und Naturwissenschaften</publisher><subject>Animals ; Anticoagulants - administration & dosage ; Anticoagulants - pharmacology ; Biological and medical sciences ; Blood Coagulation, Fibrinolysis and Cellular Haemostasis ; Blood coagulation. Blood cells ; Chlorides ; Coronary Artery Disease - etiology ; Coronary Artery Disease - pathology ; Coronary Artery Disease - physiopathology ; Coronary Vessels - pathology ; Disease Models, Animal ; Drug Evaluation, Preclinical - methods ; Electric Stimulation ; Factor V - genetics ; Femoral Vein - drug effects ; Femoral Vein - pathology ; Ferric Compounds ; Fundamental and applied biological sciences. Psychology ; Hematologic and hematopoietic diseases ; Heparin - administration & dosage ; Heparin - pharmacology ; Medical sciences ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Molecular and cellular biology ; Platelet diseases and coagulopathies ; Point Mutation ; Reproducibility of Results ; Venous Thrombosis - etiology ; Venous Thrombosis - pathology ; Venous Thrombosis - physiopathology</subject><ispartof>Thrombosis and haemostasis, 2005-09, Vol.94 (3), p.498-503</ispartof><rights>2005 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c588t-359d5d38124b4fd16dd81de10d9f3f972a43eae9c7c51e94a5bc78834bc6654c3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.thieme-connect.de/products/ejournals/pdf/10.1160/TH05-03-0170.pdf$$EPDF$$P50$$Gthieme$$H</linktopdf><linktohtml>$$Uhttps://www.thieme-connect.de/products/ejournals/html/10.1160/TH05-03-0170$$EHTML$$P50$$Gthieme$$H</linktohtml><link.rule.ids>314,780,784,3018,27924,27925,54559,54560</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17058725$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16268462$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cooley, Brian C.</creatorcontrib><creatorcontrib>Szema, Linda</creatorcontrib><creatorcontrib>Chen, Chao-Ying</creatorcontrib><creatorcontrib>Schwab, Jeffrey P.</creatorcontrib><creatorcontrib>Schmeling, Gregory</creatorcontrib><title>A murine model of deep vein thrombosis Characterization and validation in transgenic mice</title><title>Thrombosis and haemostasis</title><addtitle>Thromb Haemost</addtitle><description>Summary
Deep vein thrombosis (DVT) occurs with high prevalence in association with a number of risk factors, including major surgery, trauma, obesity, bed rest (>5 days), cancer, a previous history of DVT, and several predisposing prothrombotic mutations. A novel murine model of DVT was developed for applications to preclinical studies of transgenically constructed prothrombotic lines and evaluation of new antithrombotic therapies. A transient direct-current electrical injury was induced in the common femoral vein of adult C57Bl/6 mice. A non-occlusive thrombus grew, peaking in size at 30 min, and regressing by 60 min, as revealed by histomorphometric volume reconstruction of the clot. Pre-heparinization greatly reduced clot formation at 10, 30, and 60 min (p<0.01 versus non-heparinized). Homozygous FactorV Leiden mice (analogous to the clinical FactorV Leiden prothrombotic mutation) on a C57Bl/6 background had clot volumes more than twice those of wild-types at 30 min (0.121±0.018 mm
3
vs. 0.052±0.008 mm
3
, respectively; p<0.01). Scanning electron microscopy revealed a clot surface dominated by fibrin strands, in contrast to arterial thrombi which showed a platelet-dominated structure. This new model of DVT presents a quantifiable approach for evaluating thrombosis-related murine transgenic lines and for comparatively evaluating new pharmacologic approaches for prevention of DVT.</description><subject>Animals</subject><subject>Anticoagulants - administration & dosage</subject><subject>Anticoagulants - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Blood Coagulation, Fibrinolysis and Cellular Haemostasis</subject><subject>Blood coagulation. Blood cells</subject><subject>Chlorides</subject><subject>Coronary Artery Disease - etiology</subject><subject>Coronary Artery Disease - pathology</subject><subject>Coronary Artery Disease - physiopathology</subject><subject>Coronary Vessels - pathology</subject><subject>Disease Models, Animal</subject><subject>Drug Evaluation, Preclinical - methods</subject><subject>Electric Stimulation</subject><subject>Factor V - genetics</subject><subject>Femoral Vein - drug effects</subject><subject>Femoral Vein - pathology</subject><subject>Ferric Compounds</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Hematologic and hematopoietic diseases</subject><subject>Heparin - administration & dosage</subject><subject>Heparin - pharmacology</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Transgenic</subject><subject>Molecular and cellular biology</subject><subject>Platelet diseases and coagulopathies</subject><subject>Point Mutation</subject><subject>Reproducibility of Results</subject><subject>Venous Thrombosis - etiology</subject><subject>Venous Thrombosis - pathology</subject><subject>Venous Thrombosis - physiopathology</subject><issn>0340-6245</issn><issn>2567-689X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqtkU2L1TAUhosoznV051qy0Y1Wk-aj6XK4qCMMuBlBVyFNTm2GJrkm6R3019vSixcEd67CIQ_vy3lOVT0n-C0hAr-7vca8xrTGpMUPql3DRVsL2X19WO0wZbgWDeMX1ZOc7zAmgnX8cXVBRCMkE82u-naF_JxcAOSjhQnFAVmAAzqCC6iMKfo-ZpfRftRJmwLJ_dLFxYB0sOioJ2e3caWTDvk7BGeQdwaeVo8GPWV4dnovqy8f3t_ur-ubzx8_7a9uasOlLDXlneWWStKwng2WCGslsUCw7QY6dG2jGQUNnWkNJ9AxzXvTSklZb4TgzNDL6tWWe0jxxwy5KO-ygWnSAeKclZCtwKKjC_hmA02KOScY1CE5r9NPRbBaVapVpcJUrSoX_MUpd-492DN8crcAL0-AzkZPw7K-cfnMtZjLtuEL93rjyujAg7qLcwqLkX_Vuo3OZtSl6BnSn8jzPdSiX40afMxFr7OJoUAoy0cyozuCcjnPoFohlddhzia5Q1GsabjKY7xXY_HT0mX-Y1c-gHF6-ruP_gbOXdr0</recordid><startdate>20050901</startdate><enddate>20050901</enddate><creator>Cooley, Brian C.</creator><creator>Szema, Linda</creator><creator>Chen, Chao-Ying</creator><creator>Schwab, Jeffrey P.</creator><creator>Schmeling, Gregory</creator><general>Schattauer Verlag für Medizin und Naturwissenschaften</general><general>Schattauer GmbH</general><general>Schattauer</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></search><sort><creationdate>20050901</creationdate><title>A murine model of deep vein thrombosis Characterization and validation in transgenic mice</title><author>Cooley, Brian C. ; Szema, Linda ; Chen, Chao-Ying ; Schwab, Jeffrey P. ; Schmeling, Gregory</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c588t-359d5d38124b4fd16dd81de10d9f3f972a43eae9c7c51e94a5bc78834bc6654c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>Anticoagulants - administration & dosage</topic><topic>Anticoagulants - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Blood Coagulation, Fibrinolysis and Cellular Haemostasis</topic><topic>Blood coagulation. Blood cells</topic><topic>Chlorides</topic><topic>Coronary Artery Disease - etiology</topic><topic>Coronary Artery Disease - pathology</topic><topic>Coronary Artery Disease - physiopathology</topic><topic>Coronary Vessels - pathology</topic><topic>Disease Models, Animal</topic><topic>Drug Evaluation, Preclinical - methods</topic><topic>Electric Stimulation</topic><topic>Factor V - genetics</topic><topic>Femoral Vein - drug effects</topic><topic>Femoral Vein - pathology</topic><topic>Ferric Compounds</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Hematologic and hematopoietic diseases</topic><topic>Heparin - administration & dosage</topic><topic>Heparin - pharmacology</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Transgenic</topic><topic>Molecular and cellular biology</topic><topic>Platelet diseases and coagulopathies</topic><topic>Point Mutation</topic><topic>Reproducibility of Results</topic><topic>Venous Thrombosis - etiology</topic><topic>Venous Thrombosis - pathology</topic><topic>Venous Thrombosis - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cooley, Brian C.</creatorcontrib><creatorcontrib>Szema, Linda</creatorcontrib><creatorcontrib>Chen, Chao-Ying</creatorcontrib><creatorcontrib>Schwab, Jeffrey P.</creatorcontrib><creatorcontrib>Schmeling, Gregory</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><jtitle>Thrombosis and haemostasis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cooley, Brian C.</au><au>Szema, Linda</au><au>Chen, Chao-Ying</au><au>Schwab, Jeffrey P.</au><au>Schmeling, Gregory</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A murine model of deep vein thrombosis Characterization and validation in transgenic mice</atitle><jtitle>Thrombosis and haemostasis</jtitle><addtitle>Thromb Haemost</addtitle><date>2005-09-01</date><risdate>2005</risdate><volume>94</volume><issue>3</issue><spage>498</spage><epage>503</epage><pages>498-503</pages><issn>0340-6245</issn><eissn>2567-689X</eissn><coden>THHADQ</coden><abstract>Summary
Deep vein thrombosis (DVT) occurs with high prevalence in association with a number of risk factors, including major surgery, trauma, obesity, bed rest (>5 days), cancer, a previous history of DVT, and several predisposing prothrombotic mutations. A novel murine model of DVT was developed for applications to preclinical studies of transgenically constructed prothrombotic lines and evaluation of new antithrombotic therapies. A transient direct-current electrical injury was induced in the common femoral vein of adult C57Bl/6 mice. A non-occlusive thrombus grew, peaking in size at 30 min, and regressing by 60 min, as revealed by histomorphometric volume reconstruction of the clot. Pre-heparinization greatly reduced clot formation at 10, 30, and 60 min (p<0.01 versus non-heparinized). Homozygous FactorV Leiden mice (analogous to the clinical FactorV Leiden prothrombotic mutation) on a C57Bl/6 background had clot volumes more than twice those of wild-types at 30 min (0.121±0.018 mm
3
vs. 0.052±0.008 mm
3
, respectively; p<0.01). Scanning electron microscopy revealed a clot surface dominated by fibrin strands, in contrast to arterial thrombi which showed a platelet-dominated structure. This new model of DVT presents a quantifiable approach for evaluating thrombosis-related murine transgenic lines and for comparatively evaluating new pharmacologic approaches for prevention of DVT.</abstract><cop>Stuttgart</cop><pub>Schattauer Verlag für Medizin und Naturwissenschaften</pub><pmid>16268462</pmid><doi>10.1160/TH05-03-0170</doi><tpages>6</tpages></addata></record> |
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| ispartof | Thrombosis and haemostasis, 2005-09, Vol.94 (3), p.498-503 |
| issn | 0340-6245 2567-689X |
| language | eng |
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| source | MEDLINE; Thieme Connect Journals |
| subjects | Animals Anticoagulants - administration & dosage Anticoagulants - pharmacology Biological and medical sciences Blood Coagulation, Fibrinolysis and Cellular Haemostasis Blood coagulation. Blood cells Chlorides Coronary Artery Disease - etiology Coronary Artery Disease - pathology Coronary Artery Disease - physiopathology Coronary Vessels - pathology Disease Models, Animal Drug Evaluation, Preclinical - methods Electric Stimulation Factor V - genetics Femoral Vein - drug effects Femoral Vein - pathology Ferric Compounds Fundamental and applied biological sciences. Psychology Hematologic and hematopoietic diseases Heparin - administration & dosage Heparin - pharmacology Medical sciences Mice Mice, Inbred C57BL Mice, Transgenic Molecular and cellular biology Platelet diseases and coagulopathies Point Mutation Reproducibility of Results Venous Thrombosis - etiology Venous Thrombosis - pathology Venous Thrombosis - physiopathology |
| title | A murine model of deep vein thrombosis Characterization and validation in transgenic mice |
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