Andrew R Ednie, PhD

Department:
NeuroSci Cell Bio Physiology-SOM
Title:
Associate Professor
Address:
NEC Building 351, 3640 Colonel Glenn Hwy, Dayton, OH 45435-0001

Education and Training

Postdoctoral Fellow, Biomedical Sciences

University of South Florida, Tampa, FL (2013–2016)

Ph.D., Biomedical Sciences

University of South Florida, Tampa, FL (2012)

M.S., Molecular Medicine

University of South Florida, Tampa, FL (2011)

B.S., Microbiology and Cell Science

University of Florida, Gainesville, FL (2005)

Analytical Chemist

King Pharmaceuticals, St. Petersburg, FL (2006–2008)

MiMedx, Tampa, FL (2008)

 

Research Overview

My research program focuses on understanding how post-translational modifications regulate cardiac function in health and disease. The heart relies on precisely coordinated electrical, mechanical, and biochemical signaling to maintain normal performance, and many of these processes are controlled by reversible protein modifications. My laboratory investigates how O-GlcNAcylation, glycosylation, phosphorylation, ubiquitination, and related signaling mechanisms regulate ion channels, signaling pathways, and excitation–contraction coupling in the myocardium.

A major focus of the laboratory is defining the role of intracellular O-GlcNAcylation in cardiomyocyte excitation–contraction coupling. O-GlcNAcylation is a dynamic protein modification that functions as a cellular nutrient and stress sensor. Using integrated molecular, biochemical, electrophysiological, and animal model approaches, we investigate how O-GlcNAc signaling regulates calcium entry, calcium handling, ion channel function, and myocardial contractility. Our work has demonstrated that O-GlcNAcylation is an important regulator of cardiac excitation–contraction coupling and contributes to the heart’s ability to respond to physiological and pathological stress.

A second area of investigation seeks to define how O-GlcNAcylation influences stress-responsive signaling pathways in the heart. Current studies focus on the TAB1/p38 MAP kinase signaling axis, a critical mediator of cellular responses to injury and stress. We are investigating how O-GlcNAc modification of TAB1 alters p38 activation and downstream signaling networks, with the goal of understanding how metabolic status and post-translational modification shape cardiac stress responses.

The laboratory also investigates how extracellular protein glycosylation regulates cardiac electrical signaling and myocardial function. In collaboration with Dr. Eric Bennett and others, we have developed experimental models demonstrating that disruption of protein glycosylation profoundly affects cardiac electrical signaling, calcium handling, myocardial function, and the development of heart failure. These studies have established glycosylation as a critical regulator of cardiovascular health and continue to provide new insight into how glycans influence ion channels and signaling proteins in the heart.

Collectively, our research seeks to define how post-translational modifications integrate metabolic, electrical, and signaling pathways to regulate cardiac function. By identifying the molecular mechanisms that govern ion channel activity, intracellular signaling, and myocardial adaptation, we aim to advance fundamental understanding of cardiovascular biology and uncover new therapeutic opportunities for cardiovascular disease.

 

Experimental and Analytical Approaches

To address these questions, our laboratory integrates molecular, cellular, physiological, and computational approaches spanning protein biochemistry, cardiac electrophysiology, and whole-heart functional analysis.

  • Whole-cell patch-clamp electrophysiology
  • Cardiomyocyte calcium imaging and excitation–contraction coupling analyses
  • Protein biochemistry, molecular biology, and signal transduction studies
  • Analysis of protein glycosylation and other post-translational modifications
  • Proteomic and glycoproteomic approaches
  • Transgenic and inducible mouse models of cardiovascular disease
  • Echocardiography for assessment of cardiac structure and function
  • Surface electrocardiography (ECG) and in vivo electrophysiological phenotyping
  • Optical mapping of cardiac electrical activity and conduction
  • Ex vivo heart perfusion and functional assessment
  • Computational and systems-level modeling of cardiac signaling and electrophysiology

 

Research Interests

Post-translational modifications, O-GlcNAcylation, glycosylation, cardiac electrophysiology, excitation–contraction coupling, ion channel regulation, cardiovascular signaling, calcium handling, heart failure, arrhythmias, and cardiac stress responses.

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