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Joel Moake MD

Joel Moake MD

Senior Research Scientist and Associate Director, J. W. Cox Biomedical Engineering Laboratory, Rice University; Professor of Medicine Emeritus (Hematology), Baylor College of Medicine, Houston, Texas

Joel Moake, MD, has done clinical and basic research in hemostasis-thrombosis for more than 40 years. His special interests have been: (1) shear stress-induced, von Willebrand factor (VWF)-mediated platelet adhesion/aggregation; (2) the pathophysiology and therapy of thrombotic thrombocytopenic purpura (TTP), the hemolytic-uremic syndromes (HUS), and other types of thrombotic microangiopathies; (3) the cellular site of production of coagulation factor VIII (FVIII) and other coagulation proteins; and (4) molecular interactions between VWF and the alternative complement pathway My research team was the first to determine that: high shear stress-induced platelet adhesion/aggregation requires large human VWF multimers, as well as platelet glycoproteins Ib and IIb-IIIa, adenosine diphosphate (ADP) and calcium (1986); ultra-large (or unusually large) VWF (ULVWF) multimers secreted from endothelial cells are not processed properly, and cause systemic platelet aggregation, in thrombotic thrombocytopenic purpura (TTP, 1982); inhibition of the VWF-cleaving protease, ADAMTS-13, by Shiga toxin contributes to ULVWF-mediated thrombosis in the microcirculation of the kidney in the common enterohaemorrhagic E. coli-associated type of HUS (2002); the alternative complement pathway is initiated and amplified by C3 binding to ULVWF multimers secreted by, and anchored to, human endothelial cells (2013; FVIII is produced and stored (along with VWF) in human endothelial cell Weibel-Palade bodies (2015); and, in addition to FVIII, other coagulation factors are predominantly produced in human endothelial cells (2019-20). The 2013 discovery provides a molecular linkage between hemostasis-thrombosis and inflammation. The 2015 and 2019-20 findings suggest a new mechanism for the activation of the intrinsic coagulation pathway on endothelial cell surfaces, and the activation of the extrinsic coagulation pathways on vascular fibroblasts.


Dr. Moake has no relevant disclosures.