Faculty of Medicine, Dentistry and Health Sciences Department of Medicine, St Vincent's Hospital

Inflammation, Thrombosis and Phosphoinositide Signalling

Our research

Inflammation and coagulation operate in a feed-back loop. Inflammation leads to activation of coagulation and reciprocally coagulation can also amplify an inflammatory process. Both systems have protective roles, but on deregulation they contribute to the pathogenesis of cardiovascular disease as well response to sepsis. Thrombin, the key regulator of thrombosis, has been shown to have a pro-inflammatory activity by several mechanisms including release of cytokines from leukocytes, activation of PARs, and activation of platelets, which in turn release inflammatory mediators. My laboratory studies the role of natural anticoagulant mechanisms that function to negatively regulate thrombosis and suppress inflammation. Two pivotal pathways are of our interest: First, the thrombomodulin-endothelial protein C receptor (EPCR)-mediated generation of activated Protein C (aPC) by the action of thrombin, and second, the function of NTPDase-1/CD39 an enzyme expressed on the surface of endothelial cells and leukocytes, which exerts antithrombotic effect by hydrolysis of ADP and also exhibits anti-inflammatory activity by the consequent generation of adenosine. My group explores the effectiveness of the above two pathways using animal models that mimic human diseases of arterial and venous thrombosis, as well as inflammation induced by sepsis and immune dysfunction.

Phosphatidylinositol 3-phosphate [PtdIns(3)P] is generated from phosphatidylinositol by the action of the enzyme phosphoinositide (PI) 3-kinase. PtdIns(3)P plays a key role in the regulation of protein trafficking within the cell. Myotubularin is a PtdIns 3-phosphatase that hydrolyses PtdIns(3)P and terminates its signalling function. 3-Phosphatase adapter protein (3-PAP), cloned in my laboratory, forms a heterodimer with myotubularin and regulates muscle development. We are analyzing the physiological importance of 3-PAP by generating and analyzing mice with targeted deletion of this gene.

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Contact - enquiries @ medstv.unimelb.edu.au

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