Carol Casey, Ph.D.

Carol Casey, Ph.D.Professor, Internal Medicine Gastroenterology & Hepatology

Academic office:
Omaha VA Medical Center
4101 Woolworth Ave
Omaha, NE 68105

University of Minnesota/Duluth, Duluth, MN, Post-doctoral, 1984
Rice University, Houston TX, PhD, 1980
Augustana College, Sioux Falls, SD, BA, 1976

Areas of Interest:
I have been actively involved in the field of alcoholic liver injury for more than 30 years, with special emphasis on alcohol’s deleterious effects on protein trafficking. Our laboratory is well known for its contributions in this area, especially on a role for functional asialoglycoprotein receptor in the pathogenesis of liver injury. In particular, I have used in vitro biochemical-based experimentation combined with in vivo animal models to define important effects of toxin exposure (including ethanol exposure) on endocytic internalization and recycling of hepatocyte receptors. Our current work has extended the studies on alcohol-induced alterations in protein trafficking to alcohol’s effects on lipid droplet trafficking. In these studies we are part of a MPI-NIAAA funded program to provide a comprehensive approach using biochemical, cell biological, imaging, and animal-based methods toward understanding how ethanol consumption and/or administration affects the dynamics of lipid droplets in hepatocytes. In addition to my role as a Principal Investigator on an NIH grant, and my role as a VA Research Career Scientist, I have been actively involved in mentoring young investigators.

Selected Publications
Rasineni, K, Penrice, D, Natarajan, S, McNiven, M, McVicker, B, Kharbanda, K, Casey, C, Harris, E. Alcoholic versus non-alcoholic fatty liver: Differences in function and content of proteins involved in vesicle trafficking and receptor-mediated endocytosis. BMC Gastroenterology, 2016, 16:27, DOI:10.1186/s12876-016-0433-4 URL:

Casey, C.A., Ganapati, B, Holzapfel, M, and Petrosyan, A. Ethanol-induced Golgi disorganization:super-resolution imaging reveals the mechanisms responsible for impaired N-glycosylation. Alcohol: Clinical and Experimental Research, 17 OCT 2016 | DOI: 10.1111/acer.13247

Schulze, R, Rasineni, K, Weller, S, Casey, C, McNiven, M,. Ethanol exposure inhibits hepatocellular lipophagy by inactivating the small regulatory GTPase Rab 7. Hepatology Communications,Vol: 1, Pages: 140–152 DOI: 10.1002/hep4.1021 (2017)

Schulze R, Drizyte K, Casey C, McNiven, M. Hepatic Lipophagy: New Insights into the Autophagic Catabolism of Lipid Droplets in the Liver, Hepatology Communications, 2017, Vol 1, No. 5, Pages 359-369 DOI 10.1002/hep4.1056

Rasineni, K, Donohue, T., Thomes, P., Yang, L, Tuma D, McNiven, M, and Casey, C. Ethanol-induced steatosis involves impairment of lipophagy, associated with reduced Dynamin 2 activity. Hepatology Communications, DOI.1002/hep4.1063 2017
Schott, M, Rasineni, K, Weller, S, 1, Schulze R, Casey C, and McNiven, M. Hepatocellular lipolysis is induced by β-adrenergic stimulation and inhibited by ethanol exposure. Journal of Biological Chemistry, 292(28): DOI: 10.1074/jbc.M117.777748

For more publications