UPMC Children’s Neonatal Fellow Wins SPR Fellows Basic Research Award

June 10, 2021

Jo Duara, MD, MPH, was awarded a 2021 Society for Pediatric Research Fellows Basic Research Award for her work studying bladder urothelial injury.

Dr. Duara currently is a second-year perinatal-neonatal fellow in the UPMC Newborn Medicine Program. She earned her medical degree from the University of Miami Miller School of Medicine and then completed her residency in pediatrics at the Holtz Children’s Hospital, also at the University of Miami.

Dr. Duara’s research interests have been focused in epithelial cell biology, with previous work during her residency investigating the cellular mechanisms of lung cell damage due to hyperoxia.

At UPMC Children’s, Dr. Duara’s research focus has centered on bladder urothelial injury, working in the Bates Laboratory, which is led by Division of Pediatric Nephrology chief Carlton M. Bates, MD.Dr. Bates and his laboratory focus primarily on the roles of fibroblast growth factor receptors (FGFRs) and their signaling adapter proteins in the kidney and lower urinary tract using animal models. In recent years, the laboratory has focused on how FGF7/FGFR2 signaling acts in the context of bladder urothelial injury. The laboratory has evidence that exogenous FGF7 blocks Cyclophosphamide-induced apoptotic death of deeper urothelial cells, accelerates regeneration of outer Superficial cells, and leads to faster and high-fidelity repair compared to vehcile-treated mice. 

Dr. Duara’s research in the laboratory continues this work studying the genetic deletion of FGFR2 in mouse bladder urothelium and how it leads to regenerative defects after cyclophosphamide induced injury led by pathological endoreplication in Basal urothelial cells. Dr. Duara’s studies investigate if loss of ERK signaling downstream of FGFR2 is responsible for the pathological urothelial response to injury. 

Dr. Duara presented an abstract of her work at the 2021 Pediatric Academic Societies Annual Meeting under the title, “The Role of FGFR2/ERK Signaling in Urothelial Regeneration After Cyclophosphamide.”