Carl Bates, M.D.

  • Professor
  • Department of Pediatrics

Education & Training

  • MD from The Ohio State University College of Medicine, 1991
  • B.S. in Chemistry and Life Sciences from Otterbein College, 1986

Research Interest Summary

interrogates the roles of fibroblast growth factor receptors and their adapters in kidney and lower urinary tract development.

Research Categories

Research Interests

My research program is focused on genetic mouse models of kidney and urinary tract development, given that congenital kidney diseases are the leading causes of chronic kidney disease in children. One major project is focused on the role of fibroblast growth factor receptors in kidney development. Using conditional knockout and receptor point mutation approaches, we have uncovered many different roles for Fgfrs in different lineages within the kidney. Many of these mice have features that mimic structural kidney disease in children including renal aplasia, hypoplasia, and progressive cystic disease. Recently we have data showing that Fgfrs are critical for maintenance of nephron progenitors, the stem-cell like cells that eventually form nephrons in the kidney. This work has been supported by an NIH R01 grant that we recently successfully competed for. 
A second major project in the lab is focused on our observations that Fgfr2 is critical for normal ureteric bud induction, ureter function, and bladder function. Mice with deletion of Fgfr2 in the mesenchymal cells in these tissues develop high rates of vesicoureteral reflux (backflow of urine from the bladder to the kidney), ureter contractile defects, and bladder defects including high pressure, low capacity bladders. As the mice age, they develop scarring in the kidney, which mimics reflux nephropathy, another leading cause of chronic kidney disease in children. 

I have other NIH funded projects in the lab; one is as a co-principal investigator on an NIH R01 grant focused on the “megabladder” mouse that has a severe defect in bladder muscle formation, leading to in utero obstructive nephropathy, another leading cause of renal failure in children. I am also a co-investigator on an R01 investigating how bone morphogenetic proteins and fibroblast growth factor receptors interact in nephron patterning. As we have generated these mice and learned about the actions of fibroblast growth factor receptors in the kidney, we have considered examining DNA collected in children with structural kidney diseases for permutations in Fgf ligands and/or Fgf receptors (ranging from single nucleotide polymorphisms to larger copy number variations).

Representative Publications

Sims-Lucas S, Cullen-McEwen L, Eswarakumar VP, Hains DS Kish K, Brian Becknell B, Zhang J, Bertram JF, Wang F, Bates CM. Deletion of Frs2α from the ureteric epithelium causes renal hypoplasia. Am J Physiol Renal Physiol, 297 (5): F1208-19, 2009.

Hains DS, Sims-Lucas S, Carpenter A, Saha M, Murawsik I, Kish K, Gupta I, McHugh K, Bates CM. High incidence of vesico-ureteral reflux in mice with deletion of fibroblast growth factor receptor 2 in kidney mesenchyme. J Urol, 183(5): 2077-84, 2010.

Ingraham S, Saha M, Carpenter A, Robinson M, Ismail I, Singh S, Robinson ML, Bates CM, and McHugh KM. Pathogenesis of Renal Injury in the Megabladder Mouse: A Genetic Model of Congenital Obstructive Nephropathy, Pediatr Res, 68(6): 500-7, 2010.

Sims-Lucas S, Cusack B, Baust J, Eswarakumar VP, Masatoshi H, Takeuchi A, Bates CM. Fgfr1 and the IIIc isoform of Fgfr2 play critical roles in the metanephric mesenchyme mediating early inductive events in kidney development. Dev Dyn, 240, 240-9, 2011.

Sims-Lucas S, Cusack B, Eswarakumar VP, Zhang J, Wang F, Bates CM. Independent roles of Fgfr2 and Frs2α in ureteric epithelium. Development, 138(7): 1275-80, 2011.

Paredes J*, Sims-Lucas S*, Wang H, Lu W, Coley B, Gittes GK, Bates CM. Assessing vesicoureteral reflux in live inbred mice via ultrasound with microbubble contrast agent. Am J Physiol Renal Physiol, 300(5): F1262-5, 2011. (* authors contributed equally)

Sims-Lucas S*, Di Giovanni V*, Schaefer C, Cusack B, Eswarakumar VP, Bates CM. Ureteric Morphogenesis Requires Fgfr1 and Fgfr2/Frs2α Signaling in the Metanephric Mesenchyme. J Am Soc Nephrol, 23(4):607-17, 2012. (* authors contributed equally)

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. (* authors contributed equally)

Sims-Lucas S*, Schaefer C, Ho J, Logar A, Prochownik E, Gittes G, and Bates CM*. Endothelial progenitors exist within the kidney and lung mesenchyme. PLoS One. 8(2):e56062, 2013. (* co-corresponding authors)

Gattineni J, Priyatharshini A, Zhang Q, Mathews N, Bates CM, and Baum M. Regulation of Renal Phosphate Transport by FGF23 is Mediated by FGFR1 and FGFR4. Am J Physiol Renal Physiol, 306(3):F351-8, 2014.

Full List of Publications