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Monty Hughes Jr., PhD

Director, Duke University Urinary Dysfunction Laboratory
Assistant Professor in Surgery
Office: 383 MSRB 1, Durham, NC 27710
Campus Mail: DUMC 383 MSRB 1, Durham, NC 27710

 Dr. Hughes received his Ph.D. from the Medical University of South Carolina and was a post doc at both the University of North Carolina at Chapel Hill and NIH. He then joined the faculty of the University of North Carolina at Charlotte where he rose to the rank of Associate Professor (with tenure). Following a brief stint as the director of the biology division of a start-up pharmaceutical company, he joined forces with Dr. Purves at the Medical University of South Carolina to begin this lab focused on benign urinary disorders. Dr. Hughes has been at Duke since 2015. He is currently an Assistant Professor working within the Department of Surgery and Division of Urology. He serves as the Director of the Urinary Dysfunction Laboratory which studies the role of inflammation in disorders such as bladder outlet obstruction and diabetic bladder dysfunction. In association with Dr. J Todd Purves, this lab has been instrumental in demonstrating the central importance of the NLRP3 inflammasome in sensing the biochemical stressors associated with these disorders and translating them into an inflammatory signal. This signal is ultimately responsible for changes in voiding function, denervation and fibrosis.

Education and Training

  • Senior Research Scientist, Surgery / Urology, Duke University School of Medicine, 2015 - 2019
  • Ph.D., Medical University of South Carolina, 1992
  • B.S., Clemson University, 1987

Publications

Gross, S. A., J. M. Newton, and F. M. Hughes. “Decreased intracellular potassium levels underlie increased progesterone synthesis during ovarian follicular atresia.” Biol Reprod 64, no. 6 (June 2001): 1755–60. https://doi.org/10.1095/biolreprod64.6.1755.

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Perez, G. I., D. V. Maravei, A. M. Trbovich, J. A. Cidlowski, J. L. Tilly, and F. M. Hughes. “Identification of potassium-dependent and -independent components of the apoptotic machinery in mouse ovarian germ cells and granulosa cells.” Biol Reprod 63, no. 5 (November 2000): 1358–69. https://doi.org/10.1095/biolreprod63.5.1358.

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Mann, C. L., F. M. Hughes, and J. A. Cidlowski. “Delineation of the signaling pathways involved in glucocorticoid-induced and spontaneous apoptosis of rat thymocytes.” Endocrinology 141, no. 2 (February 2000): 528–38. https://doi.org/10.1210/endo.141.2.7314.

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Montague, J. W., C. D. Bortner, F. M. Hughes, and J. A. Cidlowski. “A necessary role for reduced intracellular potassium during the DNA degradation phase of apoptosis.” Steroids 64, no. 9 (September 1999): 563–69. https://doi.org/10.1016/s0039-128x(99)00034-3.

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Hughes, F. M., and J. A. Cidlowski. “Potassium is a critical regulator of apoptotic enzymes in vitro and in vivo.” In Adv Enzyme Regul, 39:157–71, 1999. https://doi.org/10.1016/s0065-2571(98)00010-7.

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Hughes, F. M., R. B. Evans-Storms, and J. A. Cidlowski. “Evidence that non-caspase proteases are required for chromatin degradation during apoptosis.” Cell Death Differ 5, no. 12 (December 1998): 1017–27. https://doi.org/10.1038/sj.cdd.4400418.

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Adachi, H., A. Adams, F. M. Hughes, J. Zhang, J. A. Cidlowski, and A. M. Jetten. “Induction of apoptosis by the novel retinoid AHPN in human T-cell lymphoma cells involves caspase-dependent and independent pathways.” Cell Death Differ 5, no. 11 (November 1998): 973–83. https://doi.org/10.1038/sj.cdd.4400445.

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Hughes, F. M., and J. A. Cidlowski. “Glucocorticoid-induced thymocyte apoptosis: protease-dependent activation of cell shrinkage and DNA degradation.” In J Steroid Biochem Mol Biol, 65:207–17, 1998. https://doi.org/10.1016/s0960-0760(97)00188-x.

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Spangelo, B. L., D. D. Farrimond, M. Thapa, C. M. Bulathsinghala, K. L. Bowman, A. Sareh, F. M. Hughes, A. L. Goldstein, and M. Badamchian. “Thymosin fraction 5 inhibits the proliferation of the rat neuroendocrine MMQ pituitary adenoma and C6 glioma cell lines in vitro.” Endocrinology 139, no. 4 (April 1998): 2155–62. https://doi.org/10.1210/endo.139.4.5935.

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