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Headshot of Nigel Key, M.B.,CH.B.,F.R.C.P.


My group collaborates with other BRC faculty on several disease-oriented projects. Although my expertise is primarily in the development and implementation of coagulation assays in human blood, many of our projects include both human and mouse components. These include studies on the vascular biology of sickle cell disease (with Rafal Pawlinski), cancer-associated thrombosis (with Nigel Mackman) and acute liver failure (with Rafal Pawlinski and Jian Liu). We also collaborate with several extramural research teams in studies of coagulopathy of trauma, and thrombosis associated with cancer and other disorders.

Maria Aleman


Research in the Aleman Lab is centered on basic mechanisms regulating erythropoiesis in health and disease. Differentiation of hematopoietic stem cells down the erythroid track requires coordinated gene expression, including RNA regulation, and accumulation of iron for hemoglobin production. Our current work focuses on a family of bifunctional proteins (poly C binding proteins) which both regulate RNA processing and chaperone iron within cells. Using biochemical, cellular, and in vivo models we explore the cross talk between iron trafficking and RNA regulation mediated by poly C binding proteins and how these activities are modulated by disease.


As a member of the UNC Blood Research Center, we are able to interact and collaborate with experts in blood coagulation and platelet biology. My lab is especially interested in investigating the contribution of the coagulation and platelets to anti-viral immune responses. Furthermore, in a collaborative effort with clinical experts of the UNC Blood Research Center, we are investigating potential pathways to improve cancer patients’ quality of life by reducing cardiotoxic side effects of highly efficient anti-cancer therapies.


Our role in the Blood Research Center (BRC) is to provide a unique perspective on the contribution of coagulation and fibrinolytic factors to a wide spectrum of disease pathologies, independent of the traditional roles of these factors in bleeding and thrombosis. We utilize mouse models to analyze specific mechanisms by which proteins such as prothrombin, fibrinogen, and plasminogen contribute to the progression of inflammatory, infectious, and malignant disease. Working with our collaborative basic science and clinical partners in the BRC provides an unparalleled opportunity for rapidly advancing our understanding of the multifaceted role of the hemostatic system in hemostasis, thrombosis, and beyond.


Bleeding and clotting disorders, and Hereditary Hemorrhagic Telangiectasia Dr. Raj Kasthuri is a clinician, researcher and clinical educator. Dr. Kasthuri’s clinical and research interests are in disorders of thrombosis and hemostasis, and Hereditary Hemorrhagic Telangiectasia. (HHT). Dr. Kasthuri is Associate Director for Clinical Research for the BRC. He is also Director of the UNC HHT Center of Excellence. He participates in and/or leads a number of clinical research studies evaluating the natural history of HHT and the evaluation of efficacy of novel therapies for the treatment of HHT. His laboratory interests include the mechanism(s) of coagulation activation in HHT, gene therapy for HHT, and he collaborates with other BRC investigators on research on mechanisms of thrombosis in cancer.


Dr. Little's clinical and research interests are in Sickle Cell Disease and erythropoiesis. We are interested in the physical properties of red cells, especially from people with sickle cell disease, under ambient and hypoxic conditions. We are using microfluidic devices in collaboration with colleagues at UNC and at CWRU to study red cells and to associate these findings with clinical phenotypes, before and after treatment. We are also part of a sickle cell disease registry, in order to capture data prospectively and pool resources with over 8 other institutions nationally.


To date, my research interests have focused primarily on the investigation of the coagulation system in inflammatory disorders with a thrombotic phenotype. There is known to be a close interplay between inflammation and coagulation, however, not all inflammation predisposes to thrombosis. My work aims to help better understand the role and mechanism(s) of coagulation activation in certain inflammatory disorders, and how this coagulation activation may lead to both increased thrombotic risk as well as heightened inflammation through positive feedback mechanisms.


I am the Director of the Francis Owen Blood Research Laboratory (FOBRL), the mission of which is to reduce human and animal suffering from bleeding, thrombosis and atherosclerosis by the study of unique, genetically-determined animal models of these diseases. The FOBRL was established in 1960 by Dr. Kenneth M. Brinkhous and has provided work and study opportunities for many undergraduate, M.D., D.V.M. and Ph.D. students, post-doctoral students, and faculty at UNC and from several institutions worldwide.


One area of interest is to investigate how the coagulation cascade contributes to the pathophysiology of neuroinflammation using mouse models of stroke and multiple sclerosis. We also study mechanisms of coagulation activation and clot formation in mouse models of sickle cell disease, and our goal is to identify the best mechanism of anti-coagulation to reduce the incidence of vaso-occlusive crisis, chronic inflammation, and end-organ damage associated with this blood disorder. The BRC enables us to interact with clinicians that are experts in sickle cell disease, which elevates the clinical relevance and impact of our research.


My lab develops microfluidic models of the blood and lymphatic vasculature for basic science and translational purposes. Specific projects relevant to the Blood Research Center are: 1) Understanding the role of Notch receptor signaling in vascular endothelial adherens junction assembly and stability; 2) A nascent collaboration with Dr. Prabir Roy-Chaudhury at the UNC Kidney center to screen patient plasma in microfluidic models of the vasculature to predict risk of cardiovascular complications in kidney disease.