Regulation of renal tubular cell apoptosis and proliferation after ischemic injury to a solitary kidney

Citation
R. Oberbauer et al., Regulation of renal tubular cell apoptosis and proliferation after ischemic injury to a solitary kidney, J LA CL MED, 138(5), 2001, pp. 343-351
Citations number
31
Categorie Soggetti
Research/Laboratory Medicine & Medical Tecnology","Medical Research General Topics
Journal title
JOURNAL OF LABORATORY AND CLINICAL MEDICINE
ISSN journal
00222143 → ACNP
Volume
138
Issue
5
Year of publication
2001
Pages
343 - 351
Database
ISI
SICI code
0022-2143(200111)138:5<343:RORTCA>2.0.ZU;2-U
Abstract
The time course and regulation of apoptosis and cellular regeneration after 30 minutes of acute ischemic injury to a single kidney was elucidated in r ats at five time points over 20 weeks. The fraction of apoptotic cells was most prominent at 1 day after the insult in the distal tubule (8% +/- 4% vs . 0% +/- 0%, acute renal failure (ARF) vs sham, respectively) and was still elevated at 7 days (2% +/- 2% vs 0% 0%). At that time, the whole kidney mR NA expression of the apoptosis inhibitory genes bcl-xL and bcl-2, as well a s that of the apoptosis promotor box, was significantly reduced. Immunohist ochemistry of kidney specimen showed suppression of bcl-2 in the distal tub ule but up-regulation in the proximal tubule, whereas bax protein was more strongly expressed in the distal tubule. Cellular proliferation started at day 1 and continued over the following 20 weeks, leading to severe tubular dilation and kidney failure. These data indicate that differential regulati on of bcl-2 family members contributes to the early apoptotic clearance of lethally injured tubular epithelial cells after ischemic injury to a solita ry kidney.