Publications in VIVO
 

Moseley, Pope

Professor, Disease Systems Biology, Copenhagen University, Copenhagen, Denmark

Positions

Dr. Moseley's research focuses on exercise physiology, particularly the role of the cellular heat shock protein (HSP) response in the adaptation of the whole organism to the complex stress of exercise. His research group made the initial observations that alterations in cellular HSP accumulation occur in exercising humans, and that a conditioning heat stress sufficient to cause HSP accumulation protects the whole organism from endotoxin exposure. Dr. Moseley uses both cellular and human exercise models to examine mechanisms of cellular adaptation,inflammation, and modulation of autophagy. These studies have included glutamine supplementation in exercising humans to augment the heat shock response and HSF-1 inhibitors in exercising humans to block the heat shock response.

 He has published more than 80 scientific papers and 16 book chapters, and holds seven U.S. Patents. He serves as the Associate Director of the NIH Clinical and Translational Science Center at UNM.

As Chair of the Department of Internal Medicine, Dr. Moseley’s vision is to sustain and grow the community of scholars that is the hallmark of academic internal medicine. During his service as Chair, he has overseen a large expansion of research, education, and clinical activities of the Department. Dr. Moseley has led the development of a strong Department governance structure based on transparency and accountability.

selected publications

research overview

  • My research focuses on the role of the cellular heat shock protein (HSP) response in the adaptation of the whole organism. In the intracellular environment, the HSPs serve as protein transporters and are associated with tolerance to a variety of stresses. Our research group made the initial observations that alterations in cellular HSP accumulation occur in humans under physiologic conditions, and that a conditioning heat stress sufficient to cause HSP accumulation protects the whole organism from endotoxin exposure.

    We have also explored the mechanisms behind the differential regulation of the heat shock response by oxidants, and demonstrated that the inability of aged organisms to accumulate HSP70 following heat stress reflects an alteration in gene regulation rather than a loss of potential to produce HSP70. Using both cellular systems and studies in the intact organism, our research group has identified gut injury and the loss of epithelial barrier integrity as early and perhaps pivotal events in the pathogenesis of heat stress.

    In contrast to the stress tolerance associated with intracellular HSP accumulation, HSPs seen in the local extracellular environment-either on the cell surface or released from injured cells-activate a potent immune/inflammatory response. HSP70 found on the surface of certain cells, principally tumor cells and virus-infected cells, is associated with Natural Killer cell killing. In addition, vaccines composed of HSP-tumor peptide complexes have shown promise in the generation of a specific cytotoxic T-lymphocyte response to implanted tumors in animals. My laboratory has focused on the mechanism of HSP70 mediated tumor cell recognition and on the development of HSP70-peptide complexes as vaccines. Our patents on methods to purify and synthesize these HSP-peptide complexes will allow us to conduct a variety of studies on the immune response to tumors, and make possible a number of studies and potential treatment applications.

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