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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

Jablonski, Elizabeth M., and Francis M. Hughes. “The potential role of caveolin-1 in inhibition of aquaporins during the AVD.” Biol Cell 98, no. 1 (January 2006): 33–42. https://doi.org/10.1042/BC20040131.

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Sokolova, I. M., S. Evans, and F. M. Hughes. “Cadmium-induced apoptosis in oyster hemocytes involves disturbance of cellular energy balance but no mitochondrial permeability transition.” J Exp Biol 207, no. Pt 19 (September 2004): 3369–80. https://doi.org/10.1242/jeb.01152.

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Jablonski, Elizabeth M., Ashley N. Webb, Nisha A. McConnell, Marcus C. Riley, and Francis M. Hughes. “Plasma membrane aquaporin activity can affect the rate of apoptosis but is inhibited after apoptotic volume decrease.” Am J Physiol Cell Physiol 286, no. 4 (April 2004): C975–85. https://doi.org/10.1152/ajpcell.00180.2003.

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Rueda, B. R., E. M. Jablonski, E. Oliva, Y. Huet-Hudson, and F. M. Hughes. “Estrogen regulation of AQP-2 expression in human uterine epithelium.” In Biology of Reproduction, 192–192. SOC STUDY REPRODUCTION, 2004.

Scholars@Duke

Jablonski, Elizabeth, Ashley Webb, and Francis M. Hughes. “Water movement during apoptosis: a role for aquaporins in the apoptotic volume decrease (AVD).” In Adv Exp Med Biol, 559:179–88, 2004. https://doi.org/10.1007/0-387-23752-6_17.

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Jablonski, Elizabeth M., Nisha A. McConnell, Francis M. Hughes, and Yvette M. Huet-Hudson. “Estrogen regulation of aquaporins in the mouse uterus: potential roles in uterine water movement.” Biol Reprod 69, no. 5 (November 2003): 1481–87. https://doi.org/10.1095/biolreprod.103.019927.

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Jablonski, E. M., N. A. McConnell, A. T. Motameni, Y. M. Huet-Hudson, and F. M. Hughes. “Estrogen regulation of the expression and function of AQPs in the mouse uterus.” In Biology of Reproduction, 68:117–18. SOC STUDY REPRODUCTION, 2003.

Scholars@Duke

McConnell, N. A., S. G. Yan, and F. M. Hughes. “FSH-induced aquaporin 8 expression in rat granulosa cells is mediated by a PKA-dependent mechanism.” In Biology of Reproduction, 68:113–14. SOC STUDY REPRODUCTION, 2003.

Scholars@Duke

Marriott, Ian, Francis M. Hughes, and Kenneth L. Bost. “Bacterial infection of osteoblasts induces interleukin-1beta and interleukin-18 transcription but not protein synthesis.” J Interferon Cytokine Res 22, no. 10 (October 2002): 1049–55. https://doi.org/10.1089/107999002760624288.

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McConnell, Nisha A., Raheela S. Yunus, Stephen A. Gross, Kenneth L. Bost, Mark G. Clemens, and Francis M. Hughes. “Water permeability of an ovarian antral follicle is predominantly transcellular and mediated by aquaporins.” Endocrinology 143, no. 8 (August 2002): 2905–12. https://doi.org/10.1210/endo.143.8.8953.

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