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ORIGINAL RESEARCH ARTICLE

Protein Kinase B, P34cdc2 Kinase, and p21 ras GTP-Binding in Kidneys of Aging Rats

Vipul V. Parekh^*, Jeff C. Falcone^*, Lisa A. Wills-Frank, Irving G. Joshua^*, Jaydev N. Dholakia and John C. Passmore^*,1

^* Department of Physiology and Biophysics, Department of Pathology, and Department of Biochemistry and Molecular Biology, University of Louisville School of Medicine, Louisville, Kentucky 40202

To whom requests for reprints should be addressed at ¹ Department of Physiology, University of Louisville, 500 South Preston Street, Rm. 1115, Louisville, KY 40202. E-mail: jcpass01{at}gwise.louisville.edu

Renal nephropathy present in male Wistar rats more than 13 months of age was reported as an indication that the rats were in renal failure. In this study, the renal tissue damage at 14 months of age in male Munich Wistar rats was similar to that reported for Wistar rats, indicating that Munich Wistar rats could be another model for study of kidney function in the aging rat. The usual renal response to injury involves increased cell division and/or reparative processes that involve tyrosine kinase activity (TyrK) and/or guanosine triphosphate-binding (G) protein signal trans-duction pathways. This study reveals the presence of renal tissue damage coinciding with significantly reduced activitiy of Ras, Akt, and p34cdc2 kinase, the signaling proteins that regulate cell division and/or growth, in renal cortical tissues of aging rats compared to young rats (P < 0.005, P < 0.005, and P< 0.001, respectively). These results suggest that proteins involved in signal transduction pathways associated with cell replication are downregulated in the aging kidney cortex at a time when renal cellular damage is also present.

Key Words: renal pathology • signal transduction • cellular integrity • cell cycling