In JoVE (1)
Other Publications (1)
Articles by Matthew E. Joseph in JoVE
Ferric Chloride-induced Canine Carotid Artery Thrombosis: A Large Animal Model of Vascular Injury Allyson L. Huttinger1, Debra G. Wheeler1, Surya Gnyawali2, David Dornbos III1, Juliana M. Layzer3, Nicholas Venetos1, Spencer Talentino1, Nicholas J. Musgrave1, Cheyenne Jones1, Camille Bratton1, Matthew E. Joseph4, Chandan Sen2, Bruce A. Sullenger3, Shahid M. Nimjee1 1Department of Neurological Surgery, Ohio State University, 2Department of Surgery, Ohio State University, 3Department of Surgery, Duke University, 4Department of Internal Medicine, Ohio State University Here, we present the modifications necessary to a well characterized and commonly used small animal ferric chloride-induced (FeCl3) carotid artery injury model for use in a large animal vascular injury model. The resulting model can be utilized for pre-clinical trial assessment of both prophylactic and thrombolytic pharmacological and mechanical interventions.
Other articles by Matthew E. Joseph on PubMed
Transgenic Swine: Expression of Human CD39 Protects Against Myocardial Injury Journal of Molecular and Cellular Cardiology. May, 2012 | Pubmed ID: 22269791 CD39 (ectonucleoside triphosphate diphosphohydrolase-1; ENTPD-1) rapidly hydrolyzes ATP and ADP to AMP; AMP is hydrolyzed by ecto-5'-nucleotidase (CD73) to adenosine, an anti-thrombotic and cardiovascular protective mediator. While expression of human CD39 in a murine model of myocardial ischemia/reperfusion (I/R) injury confers cardiac protection, the translational therapeutic potential of these findings requires further testing in a large animal model. To determine if transgenic expression of CD39 reduces infarct size in a swine model of myocardial ischemia/reperfusion injury, transgenic pigs expressing human CD39 (hCD39) were generated via somatic cell nuclear transfer and characterized. Expression of hC39 in cardiac tissue was confirmed by immunoblot and immunohistochemistry. Myocardial I/R injury was induced by intracoronary balloon inflation in the left anterior descending (LAD) artery for 60 min followed by 3 hours of reperfusion. The ischemic area was delineated by perfusion with 5% phthalo blue and the myocardial infarct size was determined by triphenyl tetrazolium chloride (TTC) staining. During ischemia, the rate-pressure product was significantly lower in control versus hCD39-Tg swine. Following reperfusion, compared to littermate control swine, hCD39-Tg animals displayed a significant reduction in infarct size (hCD39-Tg: 17.2 ± 4.3% vs.