Carlton M. Bates, MD
- Vice Chair of Basic Research, Division Director, Nephrology, and Professor of Pediatrics
Administative Assistant: Rebecca L. Ceoffe
Carl Bates received his MD degree at the Ohio State University College of Medicine in 1991. He completed a residency in Pediatrics in 1994 at Nationwide Children’s Hospital and then a fellowship in Pediatric Nephrology in 1998 at the University of Texas Southwestern (UTSW) Medical Center in Dallas. After one year as non tenure track faculty at UTSW, Bates became an assistant professor of pediatrics at The Ohio State University/Nationwide Children’s Hospital in 1999. He was promoted with tenure to associate professor in 2007. In 2008, Bates became the Division Director of Pediatric Nephrology and the Director of the Pediatric Nephrology Fellowship Program at the University of Pittsburgh and Children’s Hospital of Pittsburgh of UPMC. He was promoted to professor of pediatrics in 2014. In 2016, Bates assumed the role as vice chair of basic research in the Department of Pediatrics at the University of Pittsburgh School of Medicine.
Bates’ research is primarily focused on the role of fibroblast growth factor receptors (FGFRs) and their adapter binding proteins in kidney and lower urinary tract development and disease, using mouse models. Utilizing conditional and global knockout approaches to manipulate expression of FGFRs 1 and/or 2 and their adapter proteins, his lab has uncovered many novel roles for the receptors in multiple lineages and at different stages of kidney and lower urinary tract development. These mouse lines often mimic many of the congenital forms of kidney and bladder disease that are leading causes of renal and lower urinary tract disease in children.
Recently, the lab has focused on identifying mechanisms of and therapies for acute and chronic bladder injury. One of the models used is intraperitoneal cyclophosphamide administration that leads to a combination of necrotic and apopotic death of urothelial cells in the bladder and ultimately aberrant remodeling. The lab has found that administration of fibroblast growth factor 7 (FGF7) prior to Cyclophosphamide blocks much of the apoptotic death and accelerates regeneration of the cells that die of necrosis. Overall, FGF7 leads to accelerated and higher fidelity repair of urothelium. The lab has also found that deletion of endogenous receptors for FGF7 leads to aberrant regenerative responses characterized by pathological endoreplication of urothelial progenitor cells. The Bates lab is currently exploring other injury models (radiation, spinal cord injury), other therapies (mitochondrial preservation), and how mutations in cell cycle/DNA repair pathways affects urothelial response to injury. The lab is also interested in the inflammatory responses in the context of these various types of injury, therapies, and cell cycle/DNA repair gene mutations.
Professional and Scientific Society Memberships
- American Society of Nephrology, 1998-Present
- American Society of Pediatric Nephrology, 1998-Present
- International Society of Nephrology, 1998-Present
- International Pediatric Nephrology Association, 1998-Present
- National Kidney Foundation, 2009-Present
- Salt and Water Club, 2009-Present
- American Pediatric Society, 2010-Present
- American Physiological Society, 2011-Present
Education & Training
- BS, Chemistry and Life Science, summa cum laude, Otterbein College, 1986
- MD, summa cum laude, The Ohio State University College of Medicine, 1991
- Residency in Pediatrics, Columbus Children's Hospital-The Ohio State University, 1991-1994
- Fellowship in Pediatric Nephrology, University of Texas Southwestern Medical Center at Dallas, 1994-1998
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. PMID: 28052872, PMCID: PMC5407073.
Dangle PP, Ayyash O, Kang A, Bates CM, Fox J, Stephany H, Cannon G. Cystatin C-calculated Glomerular Filtration Rate-A Marker of Early Renal Dysfunction in Patients With Neuropathic Bladder. Urology, 100:213-217, 2017. PMID: 27542858 (No PMCID).
Narla D, Slagle S, Schaefer CM, Bushnell DS, Puri P, Bates CM. Loss of peri-Wolffian duct stromal Frs2α expression in mice leads to abnormal ureteric bud induction and vesicoureteral reflux. Pediatr Res, 82(6): p. 1022-1029, 2017. PMID: 29135976, PMCID: PMC5701656.
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. PMID: 29107072, PMCID: PMC5407073.
Desai PB, San Agustin JT, Stuck MW, Jonassen JA, Bates CM, and Pazour GJ. Ift25 Is Not a Cystic Kidney Disease Gene but Is Required for Early Steps of Kidney Development. Mech Dev, 151:10-17, 2018. PMID: 29606631, PMCID: PMC5972074.
Cargill K, Hemker SL, Clugston A, Murali A, Mukherjee E, Liu J, Bushnell D, Bodnar AJ, Saifudeen Z, Ho J, Bates CM, Kostka D, Goetzman ES, Sims-Lucas S. Von Hippel-Lindau Acts as a Metabolic Switch Controlling Nephron Progenitor Differentiation. J Am Soc Nephrol, 30(7):1192-1205, 2019. PMID: 31142573, PMCID: PMC6622426.
Airik R, Airik M, Schueler M, Bates CM, Hildebrandt F. Roscovitine blocks collecting duct cyst growth in Cep164-deficient kidneys. Kidney Int, 96(2):320-326, 2019. PMID: 31248650, PMCID: PMC6650321.
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, 190(1):108-124, 2020. PMID: 31654363, PMCID: PMC6943803.
Anslow MJ, Bodnar AJ, Cerqueira DM, Bushnell D, Shrom BE, Sims-Lucas S, Bates CM and Ho J. Increased rates of vesicoureteral reflux in mice from deletion of Dicer in the peri-Wolffian duct stroma. Pediatr Res, 88:382-390. 2020. PMID: 32015493, PMCID: PMC7396288.
Hurley E, Peoples ES, Bates CM, Hunstad DA, Barkin SL. Perspective commentary from the Society for Pediatric Research: supporting early-stage pediatric physician-scientist success. Pediatr Res, 87(5):834-838, 2020. PMID: 31896124, PMCID: pending.
Narla ST, Bushnell DS, Schaefer CM, Nouraie M, Tometich JT, Hand TW, Bates CM. Loss of fibroblast growth factor receptor 2 (FGFR2) leads to defective bladder urothelial regeneration after Cyclophosphamide injury. Am J Pathol, 2020, in press. PMCID-pending
Academic and Research Interests
- Bladder injury
- Fibroblast growth factor receptor
- Conditional knockout
NIH R01DK095748, Role of Fgfr2 in Bladder Injury and Regeneration (PI, 30% effort), 2019-2022, National Institute of Diabetes and Digestive and Kidney Diseases.
NIH T32DK091202, Research Training in Pediatric Nephrology (Program Director), 2016-2021, National Institute of Diabetes and Digestive and Kidney Diseases.
NIH K12HD052892, Molecular Basis of Pediatric Disease (Training Director), 2017-2022, Eunice Kennedy Shriver National Institute of Child Health and Human Development.
NIN T32HD071834, Research Training Program for Pediatric Subspecialty Fellows (Training Director-Interim), 2020-2021, Eunice Kennedy Shriver National Institute of Child Health and Human Development.