Carlton Bates, MD

  • Chief, Division of Pediatric Nephrology, Children’s Hospital of Pittsburgh of UPMC
  • Vice-Chair of Basic Research, Department of Pediatrics, University of Pittsburgh
  • Professor of Pediatrics and Cell Biology and Developmental Biology

Education & Training

  • Medical Degree – The Ohio State University – MD
  • Residency – The Ohio State University - Pediatrics
  • Fellowship – University of Texas Southwestern Medical Center – Pediatric Nephrology

Research Grants

NIH Grants:  T32, R01 

Research Summary

Dr. Bates studies the role of fibroblast growth factor receptors (FGFRs) in kidney and lower urinary tract development and disease. Through the use of genetically engineered mouse models, research in the Bates laboratory has identified how specific Fgfr family members and their docking proteins signal and function in renal and bladder development and postnatal diseases. He has generated many mouse models of renal dysplasia, cystic disease, and other congenital kidney and urinary tract anomalies. Recently his group has discovered novel roles for endogenous FGFR2 in regulating urothelial cell cycle in the context of bladder injury. The group has also shown that stimulating FGFR2 via its ligand, Keratinocyte Growth Factor, drives cytoprotection and early regeneration of urothelium after Cyclophosphamide injury. Dr. Bates is the Program Director for one of only five T32 grants for pediatric nephrology fellowship training and Training Director for one of only a dozen Pediatrics Department K12 grants in the country. He is dedicated to mentoring trainees at all levels from medical students to junior faculty. The Bates laboratory is ideal for trainees with an interest in fundamental developmental processes that are impaired in congenital renal and urinary tract anomalies or postnatal bladder injury (e.g., trainees interested in Nephrology, Newborn Medicine or Urology) or for trainees with an interest in FGFR biology.

Representative Publications

  1. Narla ST, Bushnell DS, Schaefer CM, Nouraie M, Bates CM. Keratinocyte Growth Factor reduces injury and leads to early recovery from Cyclophosphamide bladder injury. Am J Pathol, 2019, in press. PMCID: pending.
  2. Puri P, Schaefer CM, Bushnell D, Taglienti ME, Kreidberg JA, Yoder BK, Bates CM. Ectopic phosphorylated Creb marks dedifferentiated proximal tubules in cystic kidney disease. Am J Pathol, 188(1), 84–94, 2018. PMCID: PMC5407073.
  3. Ikeda, Y, Zabbarova I, Schaefer CM, Bushnell DS, de Groat WC, Kanai AJ, and Bates CM. Fgfr2 is integral for bladder mesenchyme patterning and function. Am J Physiol Renal Physiol, 312(4): F607-F618, 2017. PMCID: PMC5407073.
  4. Puri P, Bushnell D, Schaefer CM, Bates CM. Six2creFrs2α knockout mice are a novel model of renal cystogenesis. Sci Rep, 6: 36736, 2016. PMCID: PMC5113122.
  5. Di Giovanni V, Walker KA, Bushnell D, Schaefer C, Sims-Lucas S, Puri P, Bates CM. Fibroblast growth factor receptor-Frs2 signaling Is critical for nephron progenitors. Dev Biol, 400(1): 82–93, 2015. PMCID: PMC4361332.
  6. Walker KA*, Sims-Lucas S*, Di Giovanni VE, Schaefer C, Sunseri WM, Novitskaya T, deCaestecker MP, Chen F, and Bates CM. Deletion of fibroblast growth factor receptor 2 from the peri-Wolffian duct stroma leads to ureteric induction abnormalities and vesicoureteral reflux. PLoS One. 18(2):e56062, 2013. PMCID: PMC3567073 (* authors contributed equally)