Gender	Female
E-mail	deborah.hyink@mssm.edu
Education and Training	Ph.D., University of Alabama at Birmingham
	M.S., Clemson University
	B.S., Furman University
	Fellowship, The Johns Hopkins School of Medicine

Curriculum Vitae: http://www.mountsinai.org/supporting-files/cv/hyin...

Education and Training	Ph.D., University of Alabama at Birmingham
	M.S., Clemson University
	B.S., Furman University
	Fellowship, The Johns Hopkins School of Medicine

Modeling of renal development in the mouse

The morphological patterning that occurs in renal organogenesis can affect the long-term health of a person or animal. Both genetic and environmental factors affect the size of the kidney and the total number of nephrons that will form. An in-born deficit in the number of nephrons is correlated with hypertension and chronic renal failure in humans and rats (Brenner and Mackenzie, Kidney Int Suppl 63: S124-7, 1997; Clark and Bertram, Am J Physiol 276(4 Pt 2): F485-97,1999; Merlet-Benichou, Gilbert et al., Lab Invest 79(5): 515-27, 1999). However, the relationship between nephron number and adult hypertension may be more complex and may include patterns in spatial arrangement of nephrons and the vasculature or in gene and protein expression domains. The difficulty in detecting these patterns reflects the complex nature of renal development, lack of quantitative morphology, and lack of tools to examine spatial relationships between morphological structures in the kidney.

To address this, an object-relational database is being created that permits modeling of renal development in the mouse. Ureteric bud branching, position of nephrons, and branching of blood vessels are being examined in fetal mouse kidneys. We are collecting high-quality three dimensional image sets of fetal mouse kidneys using 2-photon microscopy and extracting morphological features using image analysis software. Data from these image sets will be entered into the database and will be analyzed to determine the normal spatial arrangement of the nephrons several strains of mice. Future experiments will examine the spatial patterning of mouse strains with defective renal development, including polycystic kidney disease.

Hyink DP, Abrahamson DR. Origin of the glomerular vasculature in the developing kidney. Seminars Nephrol 1995; 15: 300-314.

Robert B, St. John PL, Hyink DP, Abrahamson DR. Evidence that embryonic kidney cells expressing flk-1 are intrinsic, vasculogenic angioblasts. Am J Physiol 1996; 271: F744-F753.

Hyink DP, Tucker DC, St. John PL, Leardkamolkarn V, Accaviti MA, Abrass CK, Abrahamson DR. Endogenous origin of glomerular endothelial and mesangial cells in grafts of embryonic kidneys. Am J Physiol 1996; 270: F886-F899.

Abrahamson DR, Robert B, Hyink DP, St. John PL, Daniel TO. Origins and formation of microvasculature in the developing kidney. Kidney Int Suppl. 1998 Sep; 67: S7-11.

Hosono S, Luo X, Hyink DP, Schnapp LM, Wilson PD, Burrow CR, Reddy JC, Atweh GF, Licht JD. WT1 expression induces features of renal epithelial differentiation in mesenchymal 3T3 fibroblasts. Oncogene 1999; 18: 417-427.

Hyink DP, Rappoport JZ, Wilson PD, Abramson RG. Expression of the urate transporter/channel is developmentally regulated in human kidneys. Am J Physiol 2001; 281: F875-F886.

Gross I, Morrison DJ, Hyink DP, Georgas K, English MA, Mericskay M, Hosono S, Sassoon D, Wilson PD, Little M, Licht JD. The receptor tyrosine kinase regulator Sprouty1 is a target of the tumor suppressor WT1 and important for kidney development. J Biol Chem 2003 Oct 17; 278(42): 41420-41430.

Kaletta T, Bogaert T, Van der Craen M, Van Geel A, Dewulf N, Buechener M, Barstedt R, Hyink DP, Li H, Geng L, Burrow CR, Wilson PD. Towards understanding the polycystins. Nephron 2003; 93: E9-E17.