Abstract: A method render endothelial cells capable of inhibiting platelet and leukocyte-mediated injury and inflammation is described, comprising genetically modifying the cells by inserting DNA encoding ecto-ATP diphosphohydrolase or an oxidation-resistant analog thereof, and expressing a protein having functional ecto-ATP diphosphohydrolase activity, such as the human CD39 protein, by said cells under cellular activating conditions. The method, which can be carried out in vivo, ex vivo or in vitro, has use in allogeneic or xenogeneic transplantation as well as to treat systemic or local inflammatory conditions characterized by platelet aggregation leading to thrombus formation.

Abstract: A method to render endothelial cells capable of inhibiting platelet and leukocyte-mediated injury and inflammation is described, comprising genetically modifying the cells by inserting DNA encoding ecto-ATP diphosphohydrolase or an oxidation-resistant analog thereof, and expressing a protein having functional ecto-ATP diphosphohydrolase activity, such as the human CD39 protein, by said cells under cellular activating conditions. The method, which can be carried out in vivo, ex vivo or in vitro, has use in allogeneic or xenogeneic transplantation as well as to treat systemic or local inflammatory conditions characterized by platelet aggregation leading to thrombus formation.

Abstract: The present invention relates to the treatment of disorders using heme oxygenase-1 and heme degradation products.

Abstract: Biologically active agents covalently linked to a polymer. The polymer is preferably a biodegradable polymer are provided. The biologically active agent is preferably a protein, such as an extracellular soluble protein, e.g., an extracellular enzyme. The enzyme can be an apyrase, e.g., NTPDase. Conjugates of the invention can be used as therapeutics in subjects. For example, a conjugate comprising an apyrase can be used for treating and preventing thrombosis, atherosclerotic plaque complications and vascular disorders.

Abstract: The invention features methods of identifying a compound capable of modulating angiogenesis. Further features of the invention are methods of promoting or inhibiting angiogenesis. Methods for the diagnosis of a CD39-associated condition and for determining the prognosis of a patient diagnosed with a CD39-associated condition are also disclosed.

Abstract: The invention features methods for reducing, treating, or preventing autoimmune disorders by administering NTDPases, or alternatively, P2 receptor inhibitors to a mammal in need thereof. The invention also features methods for diagnosing a mammal as having or at risk of having an autoimmune disorder by detecting the biological activity of NTPDases or P2 receptors. Also disclosed are screening methods that make use of NTPDases and P2 receptors for the identification of novel therapeutics for autoimmune disorders.

Abstract: A method to render endothelial cells capable of inhibiting platelet and leukocyte-mediated injury and inflammation is described, comprising genetically modifying the cells by inserting DNA encoding ecto-ATP diphosphohydrolase or an oxidation-resistant analog thereof, and expressing a protein having functional ecto-ATP diphosphohydrolase activity, such as the human CD39 protein, by said cells under cellular activating conditions. The method, which can be carried out in vivo, ex vivo or in vitro, has use in allogeneic or xenogeneic transplantation as well as to treat systemic or local inflammatory conditions characterized by platelet aggregation leading to thrombus formation.

Abstract: A method of inhibiting complement activation, particularly by a transplanted tissue, in a warm-blooded vertebrate. The method includes administering a therapeutically effective amount of a platelet activity modulator to a warm-blooded vertebrate before, during or after a tissue is transplanted to the warm-blooded vertebrate, whereby complement activation by the transplanted tissue is inhibited. The platelet activity modulator can include a combination of a GPIb modulator and a GPIIb/GPIIIa modulator.

Abstract: A method of inhibiting complement activation, particularly by a transplanted tissue, in a warm-blooded vertebrate. The method includes administering a therapeutically effective amount of a platelet activity modulator to a warm-blooded vertebrate before, during or after a tissue is transplanted to the warm-blooded vertebrate, whereby complement activation by the transplanted tissue is inhibited. The platelet activity modulator can include a combination of a GPIb modulator and a GPIIb/GPIIIa modulator.