Removal of one kidney in numerous mammalian species, including man, provokes metabolic changes within a few minutes that can lead ultimately to complete restoration of renal function and doubling of the mass of the remaining kidney. In its rapidity, completeness of growth without the necessity for mitosis, and freedom form artefacts caused by injury to the organ being studied, compensatory renal hypertrophy is a unique system in which to analyze the mechanisms that control growth in general and renal growth, in particular. Identification of growth-regulatory substances might lead to their being used to induce new renal growth in patients with renal insufficiency. Examined from the other extreme, acute renal insufficiency might represent a malfunction of the processes of renal hypertrophy that normally repair the effects of renal injury. The intent of these studies is to characterize the regulation of macromolecular synthesis in compensatory hypertrophy and in renal damage produced by ischemia or cisplatin. Aspects to be examined include determination of whether or not: 1. new ribosomal RNA transcription units are activated 2. availability of RNA polymerase-I transcription factors limits rRNA gene transcription 3. the rate of transfer RNA gene transcription is stimulated by contralateral nephrectomy 4. novel messenger RNAs accumulate 5. regulatory events in compensatory hypertrophy are also concomitants of recovery form injury 6. mitochondrial proliferation and gene expression are components of recovery 7. effects of ischemia on renal proteins are controlled by genetic mechanisms.
| Witzgall, R; O'Leary, E; Gessner, R et al. (1993) Kid-1, a putative renal transcription factor: regulation during ontogeny and in response to ischemia and toxic injury. Mol Cell Biol 13:1933-42 |
| Ouellette, A J; Malt, R A; Sukhatme, V P et al. (1990) Expression of two ""immediate early"" genes, Egr-1 and c-fos, in response to renal ischemia and during compensatory renal hypertrophy in mice. J Clin Invest 85:766-71 |
