The objective of this study is to further develop previous work done on this project on reaction to injury in the kidney by focusing specifically on the pathophysiology of acute renal failure using an ischemic and toxic model. The focus of the research is on the pathophysiology of reversible and irreversible cellular changes in the proximal convoluted tubule which we believe to be the key to the initiation phase of acute renal failure and on the subsequent interactions involving the juxtaglomerular apparatus. The problem will be approached correlating structure, function and biochemical information and an important facet of the strategy is to extend results developed on whole kidney in vivo models of ischemia and to isolate single proximal tubular cells. Because of the heterogeneous nature of the kidney cortex and difficulties in interpreting biochemical data, this is of great importance.

Agency
National Institute of Health (NIH)
Institute
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Type
Research Project (R01)
Project #
5R01DK015440-15
Application #
3225400
Study Section
Pathology A Study Section (PTHA)
Project Start
1980-01-01
Project End
1988-06-30
Budget Start
1987-01-01
Budget End
1988-06-30
Support Year
15
Fiscal Year
1987
Total Cost
Indirect Cost
Name
University of Maryland Baltimore
Department
Type
Schools of Medicine
DUNS #
003255213
City
Baltimore
State
MD
Country
United States
Zip Code
21201
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Best, C J; Tanzer, L R; Phelps, P C et al. (1999) H-ras-transformed NRK-52E renal epithelial cells have altered growth, morphology, and cytoskeletal structure that correlates with renal cell carcinoma in vivo. In Vitro Cell Dev Biol Anim 35:205-14
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Trump, B F; Berezesky, I K; Chang, S H et al. (1997) The pathways of cell death: oncosis, apoptosis, and necrosis. Toxicol Pathol 25:82-8
Amstad, P A; Liu, H; Ichimiya, M et al. (1997) bcl-2 enhancement of malignant transformation in mouse epidermal JB6 cells. Mol Carcinog 20:231-9
Davis, M A; Chang, S H; Trump, B F (1996) Differential sensitivity of normal and H-ras oncogene-transformed rat kidney epithelial cells to okadaic acid-induced apoptosis. Toxicol Appl Pharmacol 141:93-101
Gu, H; Smith, M W; Phelps, P C et al. (1996) H-ras transfection of the rat kidney cell line NRK-52E results in increased induction of c-fos, c-jun and hsp70 following sulofenur treatment. Cancer Lett 106:199-205
Trump, B F; Berezesky, I K (1996) The mechanisms of calcium-mediated cell injury and cell death [correcgted] New Horiz 4:139-50

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