A photo of Cristina Cebrian.

Assistant Professor, UC Department of Pediatrics

513-803-0470

Biography & Affiliation

Biography

My research interests are kidney development and disease. The kidney is a remarkable organ with multiple functions — not only filtering the blood and removing waste products in the urine, but also regulating blood pressure, balancing the body’s fluids, controlling red blood cell production and promoting strong, healthy bones by producing vitamin D.

Typical treatments for mild kidney disease include taking medication and diet changes. However, when the kidneys no longer function, dialysis and receiving a kidney transplant are the only treatments. Due to the serious symptoms associated with this disease and lack of a permanent cure, researchers must continue studying how the kidneys work and identifying ways to regenerate a diseased kidney.

The nephrons are the filtering units of the kidney and a single human kidney has, on average, 1 million nephrons that are formed exclusively during fetal life. When the nephrons are damaged due to disease, or if you are born with fewer nephrons, the remaining ones have to compensate. This often results in further kidney damage and disease.

My research team and I are attempting to learn about and understand how the kidneys generate the correct number of nephrons. We are doing so by studying the cellular and molecular systems that stimulate kidney development and the significance of flaws in these systems. In addition, we are also studying a common disease of the kidney known as polycystic kidney disease. Patients with this disease gradually lose kidney function because a number of their nephrons become cystic.

My research team is part of a highly collaborative network of kidney researchers. Our recent work includes the identification of the genes expressed in the human fetal kidney at the level of individual cells. In my previous work as a postdoctoral fellow, our team described that nephron progenitors self-restore in sync with the branching ureteric bud to regulate adult kidney size and the nephron number.

I have more than 10 years of experience in the field of developmental biology and joined the team at Cincinnati Children’s Hospital Medical Center in 2018. My research has been published in various journals, including Development, Frontiers in Physiology, Stem Cell Reports, PLoS Biology and Nature Genetics.

Academic Affiliation

Assistant Professor, UC Department of Pediatrics

Research Divisions

Developmental Biology

Education

BSc: Universitat de Barcelona, Spain.

PhD: Universitat Autònoma de Barcelona, Spain.

Postdoctoral Fellow: Weill Cornell Medical College and Columbia University, New York, NY.

Publications

Organoid single cell profiling identifies a transcriptional signature of glomerular disease. Harder, JL; Menon, R; Otto, EA; Zhou, J; Eddy, S; Wys, NL; O'Connor, C; Luo, J; Nair, V; Cebrian, C; et al. JCI insight. 2019; 4.

Regulation of Renal Differentiation by Trophic Factors. Kurtzeborn, K; Cebrian, C; Kuure, S. Frontiers in Physiology. 2018; 9.

Hox5 genes direct elastin network formation during alveologenesis by regulating myofibroblast adhesion. Hrycaj, SM; Marty-Santos, L; Cebrian, C; Rasky, AJ; Ptaschinski, C; Lukacs, NW; Wellik, DM. Proceedings of the National Academy of Sciences of USA. 2018; 115:E10605-E10614.

Dynamic MAPK/ERK Activity Sustains Nephron Progenitors through Niche Regulation and Primes Precursors for Differentiation. Ihermann-Hella, A; Hirashima, T; Kupari, J; Kurtzeborn, K; Li, H; Kwon, HN; Cebrian, C; Soofi, A; Dapkunas, A; Miinalainen, I; et al. Stem Cell Reports. 2018; 11:912-928.

Single-cell analysis of progenitor cell dynamics and lineage specification in the human fetal kidney. Menon, R; Otto, EA; Kokoruda, A; Zhou, W; Zhang, Z; Yoon, E; Chen, Y; Troyanskaya, O; Spence, JR; Kretzler, M; et al. Development (Cambridge). 2018; 145:dev164038-dev164038.

Radial WNT5A-Guided Post-mitotic Filopodial Pathfinding Is Critical for Midgut Tube Elongation. Wang, S; Cebrian, C; Schnell, S; Gumucio, DL. Developmental Cell. 2018; 46:173-188.e3.

Haploinsufficiency for the Six2 gene increases nephron progenitor proliferation promoting branching and nephron number. Combes, AN; Wilson, S; Phipson, B; Binnie, BB; Ju, A; Lawlor, KT; Cebrian, C; Walton, SL; Smyth, IM; Moritz, KM; et al. Kidney International. 2018; 93:589-598.

Ret and Etv4 Promote Directed Movements of Progenitor Cells during Renal Branching Morphogenesis. Riccio, P; Cebrian, C; Zong, H; Hippenmeyer, S; Costantini, F. PLoS Biology. 2016; 14:e1002382-e1002382.