Edward N Harris

Biography

I started my career at Louisiana State University as a graduate student studying Rab GTPases in Dictyostelium under the direction of Dr. James Cardelli.  My thesis was specifically on RabD, a Rab14 mammalian homolog, but expanded into several of the participating Rabs and some of the lysosomal trafficking regulators such as Lvs. In 2002, I started a post-doc fellowship in the laboratory of Dr. Paul H. Weigel dissecting the biochemical relationship of the HARE/Stabilin-2 receptor with the binding and endocytosis of glycosaminoglycans, primarily hyaluronan and heparin. These studies resulted in 8 papers in which I and my colleagues examined how these ligands bind, how they are competed by each other, signaling mechanisms propagated by the receptor, and so forth. I spent 8 years in Oklahoma City; 4 years as a post-doctoral fellow and 4 years as a research assistant professor.  During this time I also taught nutritional biochemistry to the Food and Nutrition undergraduate and graduate students. In 2010, I started up my own lab at the University of Nebraska.
 

Research Interest

My primary research interest is in the continual study of the Stabilin receptors and how they bind different heparinoid polymers. This ranges from basic biochemical assays for binding/competition to using animal models to examine the physiological aspects of heparin, HA, chondroitin sulfate scavenging in the liver.  The body turns over approximately 1/3 of the total hyaluronan content daily.  Heparin, which is used in all surgical procedures and in the treatment of thrombosis and dialysis, is a very diverse molecule with little understanding of how it is catabolized from the blood stream. My lab seeks to understand how the liver scavenges heparinoid molecules and what other molecules may inhibit or enhance the initial steps in this catabolic pathway. Other interests include the host liver cell of the stabilin receptors which is the sinusoidal endothelial cell (SEC) and how it behaves under metabolic stresses such as dyslipidemia and fluxes of heparin and HA. There are also interesting cross-talk pathways between SECs and hepatocytes since SEC are the guardians of the liver. They contain fenestration or cytoplasmic holes in which they act as a filter for macromolecular complexes. SECs are among the most endocytic cells in the body and their ability to internalize and catabolize the myriad amount of material from the blood has not been fully explored.