Aura Perez, M.D., Ph.D.
Assistant Professor
Aura.Perez@case.edu
BRB Room 829
(216) 368 6894 Phone
(216) 368 4223 Fax
Biography
Dr. Perez received an M.D. degree from the Pontificia Universidad Católica Madre y Maestra (PUCMM), Santiago, Dominican Republic in 1982; an M.S. in Physiology from Emory University Atlanta, GA in 1987; and a Ph.D. in Physiology from Emory University, Atlanta, GA in 1990. From 1990 to 1991, Dr. Perez did a post-doctoral fellowship in Dr. Ulrich Hopfer’s and Dr. Pamela Davis’ lab at Case Western Reserve University and Rainbow Babies and Children’s Hospital, Cleveland, OH. She was promoted to instructor in 2003. In 2005, Dr. Perez was promoted to Assistant Professor in the Department of Pediatrics.
Research Interests
Although impaired chloride transport is the basic defect in cystic fibrosis (CF), the prevalent cause of death in CF patients is the relentless, progressive, lung infection and inflammation. CF patients acquire Pseudomonas aeruginosa infection early in life leading to an intense inflammatory response that is unable to control the infection despite a massive recruitment of active phagocytes. Understanding the mechanisms that cause the excessive inflammatory response is vital in order for us to develop effective therapeutic agents, because the ideal anti-inflammatory therapeutic agent will be one whose actions are directed solely towards the “excessive” part of the inflammatory response and leave intact the “protective” part of a normal inflammatory response. For this reason, it will be important to have a broad view not only of the multifaceted responses to bacterial exposure in CF airway epithelial cells, but also of the differences from normal cells, and also to determine the broad impact of putative therapeutic agents on these responses. Even thought the CF patient dies primarily as a consequence of the destruction of their lungs by inflammation and infection; with new treatment, the life expectancy of the CF patient has increased considerably, so now doctors managing the CF patient have to pay even more attention to the other complications associated with CF: malnutrition and gastrointestinal issues. The malnutrition observed in the CF patient has been associated with a poor prognosis of their lung function in the long run, so it is essential that nutrition and/or fat absorption be improved in the CF patient. Understanding how fat is misprocessed in the CF patient will help in identifying new therapies that can be applied to improve the nutritional status of the CF patient and therefore in the long run improve the health of the lungs of the CF patient.
Publications
Perez A, van Heeckeren AM, Nichols D, Gupta S, Eastman JF, and Davis PB. “Peroxisome proliferators-activated receptor gamma in cystic fibrosis lung epithelium” Articles in PresS Am J Physiol Cell Mol Physiol (June 13, 2008).
Perez A, Issler AC, Cotton CU, Kelley TJ, Verkman AS, Davis PB.
"CFTR inhibition mimics the cystic fibrosis inflammatory profile"
Am J Physiol Lung Cell Mol Physiol. 292(2):L383-L395, 2007.
Gupta S, Heacock M, Perez A, Davis PB. “Antibodies to the polymeric immunoglobulin receptor with different binding and trafficking patterns” .Am J Respir Cell Mol Biol. 33(4):363-370, 2005.
Perez A, Davis PB. "Gene profile changes after Pseudomonas aeruginosa exposure in immortalized airway epithelial cells". J Struct Funct Genomics. 5(3):179-194, 2004.
Kube D, Adams L, Perez A, Davis PB. "Terminal sialylation is altered in airway cells with impaired CFTR-mediated chloride transport". Am J Physiol Lung Cell Mol Physiol. 280(3):L482-492, 2001.
Bryan R, Kube D, Perez A, Davis P, Prince A. "Overproduction of the CFTR R domain leads to increased levels of asialoGM1 and increased Pseudomonas aeruginosa binding by epithelial cells". Am J Respir Cell Mol Biol. 19(2):269-277, 1998.
Perez A, Risma KA, Eckman EA, and Davis PB. “Overexpression of R domain eliminates cAMP stimulated chloride secretion in 9/HTEo- cells in culture”. Am. J. Physiol. 271(15):L85-L92, 1996.
Davis PB, Silski CL, and Perez A. ”cAMP does not regulate [Ca++]i in human tracheal epithelial cells in primary culture”. J. Cell Science. 107:2899-2907, 1994. |
