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Our laboratory is interested in the development of gene-based strategies for the treatment of bleeding and thrombotic diseases. In a collaborative effort, we and others have carried out early-phase clinical studies on adeno-associated viral (AAV) vectors for the treatment of severe hemophilia B (factor IX deficiency). Current projects are focused on translational research studies on the efficacy and safety of intravascular delivery of AAV vectors to skeletal muscle or liver of dogs and mice with severe hemophilia. We are also identifying biological factors that modulate AAV vectors transduction and the risk of inadvertent germline transmission in animal models.
Blockage of blood vessels causes many serious human diseases, including myocardial infarct, ischemic strokes, and venous thrombosis. They contribute to the mortality and morbidity of septic shock, chronic inflammatory injury, and vascular complications of systemic diseases. The protein C anticoagulant pathway plays a major role in the interface between coagulation and inflammatory processes. Venous thrombosis is most commonly the result of defects in the proteins that participate in the protein C anticoagulant pathway. Activated Protein C (APC) mediates anticoagulant effects and signals cellular responses that are anti-inflammatory in nature. The current notion that occlusive vascular diseases such as atherosclerosis are forms of systemic diseases in which underlying inflammatory and thrombotic processes play a critical role led us to postulate that APC could offer an alternative therapeutic option. Ongoing studies are aimed at elucidating in vivo functions of APC in a series of animal models for thrombotic and/or inflammatory diseases.
Blockage of blood vessels causes many serious human diseases, including myocardial infarct, ischemic strokes, and venous thrombosis. They contribute to the mortality and morbidity of septic shock, chronic inflammatory injury, and vascular complications of systemic diseases. The protein C anticoagulant pathway plays a major role in the interface between coagulation and inflammatory processes. Venous thrombosis is most commonly the result of defects in the proteins that participate in the protein C anticoagulant pathway. Activated Protein C (APC) mediates anticoagulant effects and signals cellular responses that are anti-inflammatory in nature. The current notion that occlusive vascular diseases such as atherosclerosis are forms of systemic diseases in which underlying inflammatory and thrombotic processes play a critical role led us to postulate that APC could offer an alternative therapeutic option. Ongoing studies are aimed at elucidating in vivo functions of APC in a series of animal models for thrombotic and/or inflammatory diseases.
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Morgan Hresko,Kavitha Muralidharan,Caroline Markmann,Lucy Li, Ralph Bunte, Enrico Radaelli,Charles-Antoine Assenmacher,Valder Arruda,Michael Milone,Benjamin Samelson-Jones,Vijay Bhoj
HAEMOPHILIAno. S3 (2021): 28-36
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