|Areas of Expertise|
Eric Wauson joined the physiology and pharmacology faculty at Des Moines University in January 2014. He received his undergraduate degree in biology from Creighton University in Omaha and his Ph.D. in pharmacology from the University of North Carolina in Chapel Hill. Prior to joining the DMU faculty, he participated in postdoctoral work with Melanie Cobb at the University of Texas Southwestern Medical Center in Dallas. Dr. Wauson studies the roles of nutrient-responsive G protein-coupled receptor (GPCR) signaling in normal physiology and pathological conditions. He utilizes a variety of biochemical and physiological approaches in both tissue culture and mouse model systems to potentially reveal novel therapeutic options for treating cardiovascular disease and cancer.
Biomedical Research Interests
Organisms require the ability to detect nutrient and energy availability to regulate metabolic homeostasis. While much remains unknown about how cells sense nutrients, studies have shown that the dysregulation of nutrient sensors may cause cardiovascular disease, obesity, cancer, diabetes and other disease states. The long term goal of my laboratory is to define the functions of the amino acid sensing G protein-coupled receptors (GPCRs) in normal physiology and pathological conditions. The detection of amino acid levels allows cells to balance catabolic processes (e.g., protein synthesis) with anabolic processes (e.g., macroautophagy, often referred to as autophagy). Autophagy is a highly regulated process by which proteins, organelles, and other cytoplasmic components are delivered to the lysosome where they are degraded into their constituents. These molecules are released from the lysosome and used in the production of energy and the synthesis of new cellular components. Studies suggest that acute autophagy induction during cardiac ischemia protects against cardiomyocyte death. The mechanistic target of rapamycin (mTOR) is an important regulator of autophagy. We have discovered that amino acids stimulate the GPCR T1R1/T1R3 to activate mTOR and inhibit autophagy in numerous cell lines including cardiomyocytes. We currently utilize a variety of biochemical and physiological approaches in both tissue culture and mouse model systems to determine how T1R1/T1R3 regulates autophagy and other cellular processes during cardiovascular disease states. This research is expected to reveal novel therapeutic options for treating myocardial infarction and other cardiovascular diseases.
Wauson EM, Dbouk HA, Ghosh AB, and Cobb MH. Autophagy and the interplay between nutrients and G protein-coupled receptors. (Invited review submitted to Trends in Endocrinology and Metabolism) , 2013
Wauson EM, Guerra ML, Barylko B, Albanesi JP, and Cobb MH. Off-Target Effects of MEK Inhibitors. Biochemistry. 2013 Aug 6; 52(31):5164-6. , 2013
Wauson EM, Lorente-Rodriguez A, and Cobb MH. (Invited review). Minireview: Nutrient Sensing by G Protein-Coupled Receptors. Mol Endocrinol. 2013 Aug; 27(8): 1188-97., 2013
Wauson EM, Zaganjor E, and Cobb MH. Amino acid regulation of autophagy through the GPCR TAS1R1-TAS1R3. Autophagy. 2013 March; 9(3): 418-419., 2013
Wauson EM, Zaganjor E, Lee A, Guerra ML, Ghosh AB, Bookout AL, Chambers CP, Jivan A, McGlynn K, Hutchison M, Deberadinis RJ, and Cobb MH. The G protein-coupled taste receptor T1R1/T1R3 regulates mTORC1 and autophagy. Molecular Cell. 2012 Sep 28; 47(6): 851-862. (Featured Article), 2013
Bodemann BO, Orvedahl A, Cheng T, Ram RR, Ou YH, Formstecher E, Maiti M, Hazelett CC, Wauson EM, Balakireva M, Camonis JH, Yeaman C, Levine B, White MA. RalB and the exocyst mediate the cellular starvation response by direct activation of autophagosome assembly. Cell. 2011 Jan 21;144(2): 253-267. , 2011
Dioum EM, Wauson EM, Cobb MH. MAP-ping unconventional protein-DNA interactions. Cell 2009 Oct 30; 139(3): 462-463. , 2009
Lindsey-Boltz LA*, Wauson EM*, Graves LM, Sancar A. (2004) The human Rad9 checkpoint protein stimulates the carbamoyl phosphate synthetase activity of the multifunctional protein CAD. Nucleic Acids Res. 32(15): 4524-4530. *Co-first authors. , 2004
Wauson EM, Langan AS, Vorce RL. Sodium arsenite inhibits and reverses expression of adipogenic and fat cell-specific genes during in vitro adipogenesis. Toxicological Sciences. 2002; 65(2): 211-219. , 2002
Ruan Y, Peterson MH, Wauson EM, Waes JG, Finnell RH, and Vorce RL. Folic acid protects SWV/Fnn embryo fibroblasts against arsenic toxicity. Toxicological Letters. 2000; 117(3): 129-137. , 2000
Trouba KJ, Wauson EM, and Vorce RL. Sodium arsenite inhibits terminal differentiation of murine C3H-10T1/2 preadipocytes. Toxicol. Appl. Pharmacol. 2000; 169(1): 25-35., 2000
Trouba KJ, Wauson EM, and Vorce RL. Sodium arsenite-induced dysregulation of proteins involved in proliferative signaling. Toxicol. Appl. Pharmacol. 2000; 164(2): 161-170. , 2000