Mouse models of sickle cell disease, drug-induced liver injury, and endotoxemia.
Education and Experience
BS Cum Laude: Allegheny College, 2005; PhD (Pharmacology and Toxicology): Michigan State University, 2011; Postdoctoral Fellowship: University of North Carolina, 2011-2016; Research Associate: University of North Carolina, 2016-2019; Assistant Professor of Medicine: University of North Carolina 2019-present.
Research and Clinical Interests
I am interested in studying the cross-talk between coagulation and inflammation in various animal models of disease, including sickle cell disease, thrombosis, and drug-induced liver injury. My current focus is to target the coagulation cascade and protease activated receptors to reduce the incidence and severity of vaso-occlusive crisis in sickle cell disease. Another area of interest is determining the role of the intrinsic coagulation cascade in the pathophysiology and end-organ damage associated with sickle cell disease.
Sparkenbaugh EM, Chen C, Brzoska T, Nguyen J, Wang S, Vercellotti G, Key NS, Sundd P, Belcher J, and Palwinski R. Thrombin-mediated activation of PAR-1 contributes to microvascular stasis in mouse models of sickle cell disease. Blood. 2020. DOI: 10.1182/bloo,2019003543.
Sparkenbaugh EM, Chantrathammachart P, Chandarajoti K, Mackman N, Key NS, and Pawlinski R. Blood. 127(10): 1371. 2016.
Sparkenbaugh EM, Chantrathammachart P, Mickelson J, van Ryn J, Hebbell R, Monroe DM, Mackman N, Key NS, Pawlinski R. Blood. 123(11): 1747. 2014.