John Fenimore

Participant: PROMISE AGEP Research Symposium

John Fenimore

Department: Biological Sciences

Institution: University of Maryland, Baltimore County (UMBC)



Cardiac Muscular Changes Driven by IFN- Exposure

Authors: John Fenimore, Rebecca Erwin-Cohen, Julio Valencia, Danielle Springer, Erika Palmieri, Elijah Edminston, Michael N. Sack, Javid Moslehi, Dan McVicar and Howard Young.


The effect of cytokines on non-traditional immunological targets is a point of continual study. Cardiovascular myopathies have been associated with a chronic inflammatory response and activated cell-mediated immunity. Our findings, as generated via observation of in vivo and in vitro cardiovascular activity during the expression of a low persistent level of IFN- in mutant mice (ARE-Del mice) and wild type levels of IFN-, indicate that the chronic expression of the cytokine results in a model for heart failure under stress. As a cause of this condition, there is possible involvement of cellular infiltrate and metabolic changes in ARE-Del-/- murine hearts due to the chronic IFN- expression causing a stress exacerbated decrease in heart function. Our data shows an increase in glucose expenditure and lactic acid production in murine models when exposed to chronic IFN-. The in vivo studies demonstrated an increase in the expression of factors associated with fatigue such as lactic acid and gene expression changes associated with an increase in anaerobic respiration in cardiac musculature. Considering that patients with many autoimmune diseases have associated fatigue, it is likely that immune dysfunction driven changes may play a critical role in the concurrence of fatigue based disorders. These studies may provide new insight into the involvement of IFN- in fatigue and cardiomyopathy.

Keywords: Myocarditis, Cytokines, Inflammation, Autoimmune Disease, Cardiomyopathy, IFN-



I am currently a Ph. D student at the University of Maryland Baltimore County and am in my first year. I have worked at LANL and the NCI in Frederick. I have done work involving the adverse effects of autoimmunity on aspects of behavior and muscular function. I have always had a great interest in the signaling mechanisms and intersections of biological systems. But observing these connections and interrelations we can clarify our understanding of complex diseases and how we deal with them effectively and what can go wrong. I have focused my research on autoimmunity, signaling and cell development and have a great interest in the intersection between host, pathogen and regulation of host response.



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