The major causes of chronic renal failure in the United States include conditions affecting the glomerulus (e.g. diabetes, FSGS, hypertension, and inflammatory glomerular disease), while those causing acute renal failure involve the renal tubule through toxic and ischemic mechanisms. Both types of renal failure are associated with high mortality and cost to the Nation. The human genome project offers enormous opportunities to understand and develop new strategies for manipulating signaling pathways and structural protein complexes that will have potential therapeutic and diagnostic utility in kidney diseases. To take advantage of these opportunities this Renal Center will have a Molecular/Morphology Core and four individual research projects. The individual projects are derived in part from prior work previously supported by the Renal Center, and will focus on newly discovered and cloned molecules which regulate glomerular structure and function (Wiggins, Wang and Margolis/Kershaw), on protein:protein: lipid interactions as they become uncontrolled and uncoordinated in the hypoxic tubule (Weinberg/Shayman), and on signaling systems involved in tubulogenesis that may be important in tubular regeneration following injury (Dressler/Dixon). A major role of the Molecular/Morphology core will be the production of high quality libraries of various types (e.g. RNA, cDNA, yeast two hybrid, full length cDNA for mammalian expression) for the dissection of protein interactions of importance in the glomerulus, tubule and developing kidney. In order to create this Core we have had to identify additional support ($400,000 over 5 years) from a private donor and the Institution. Our goal is that this Molecular/Morphology Core will be a resource that will serve both the Center projects and other investigators in our Institution as well as the renal community at large through rapid dissemination of the libraries that are developed.
| Hato, Takashi; Winfree, Seth; Day, Richard et al. (2017) Two-Photon Intravital Fluorescence Lifetime Imaging of the Kidney Reveals Cell-Type Specific Metabolic Signatures. J Am Soc Nephrol 28:2420-2430 |
| Kikuchi, Masao; Wickman, Larysa; Hodgin, Jeffrey B et al. (2015) Podometrics as a Potential Clinical Tool for Glomerular Disease Management. Semin Nephrol 35:245-55 |
| Yu, Fa-Xing; Zhao, Bin; Guan, Kun-Liang (2015) Hippo Pathway in Organ Size Control, Tissue Homeostasis, and Cancer. Cell 163:811-28 |
| Fukuda, Akihiro; Wickman, Larysa T; Venkatareddy, Madhusudan P et al. (2012) Urine podocin:nephrin mRNA ratio (PNR) as a podocyte stress biomarker. Nephrol Dial Transplant 27:4079-87 |
| Fukuda, Akihiro; Wickman, Larysa T; Venkatareddy, Madhusudan P et al. (2012) Angiotensin II-dependent persistent podocyte loss from destabilized glomeruli causes progression of end stage kidney disease. Kidney Int 81:40-55 |
| Wiggins, Jocelyn E (2012) Aging in the glomerulus. J Gerontol A Biol Sci Med Sci 67:1358-64 |
| Fukuda, Akihiro; Chowdhury, Mahboob A; Venkatareddy, Madhusudan P et al. (2012) Growth-dependent podocyte failure causes glomerulosclerosis. J Am Soc Nephrol 23:1351-63 |
| Chernin, Gil; Vega-Warner, Virginia; Schoeb, Dominik S et al. (2010) Genotype/phenotype correlation in nephrotic syndrome caused by WT1 mutations. Clin J Am Soc Nephrol 5:1655-62 |
| Chernin, Gil; Heeringa, Saskia F; Vega-Warner, Virginia et al. (2010) Adequate use of allele frequencies in Hispanics--a problem elucidated in nephrotic syndrome. Pediatr Nephrol 25:261-6 |
| Kim, Doyeob; Patel, Sanjeevkumar R; Xiao, Hong et al. (2009) The role of PTIP in maintaining embryonic stem cell pluripotency. Stem Cells 27:1516-23 |
Showing the most recent 10 out of 189 publications
