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Am J Physiol Renal Physiol 272: F640-F647, 1997;
0363-6127/97 $5.00
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AJP - Renal Physiology, Vol 272, Issue 5 640-F647, Copyright © 1997 by American Physiological Society

ARTICLES

Expression of bcl-2 and bax in regenerating rat renal tubules following ischemic injury

D. P. Basile, H. Liapis and M. R. Hammerman
George M. O'Brien Kidney and Urological Disease Center, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri 63110, USA.

To define potential roles for bcl-2 and bax in adult kidney as regulators of regeneration, their expressions were characterized postischemic injury. A 2.1-fold increase in levels of renal bcl-2 mRNA occurred within 24 h of injury relative to levels in kidney of sham-operated control rats. The levels of bcl-2 mRNA remained elevated for 3 days but returned to baseline by day 5 postischemia. In situ hybridization of kidneys from sham-operated rats demonstrated faint expression of bcl-2 mRNA localized diffusely throughout the nephron. After renal injury, the expression of bcl-2 mRNA was markedly enhanced in regenerating proximal tubule cells relining the basement membrane. Immunohistochemistry showed a similar localization for bcl-2 protein. Levels of bax mRNA in kidney were elevated beginning at 24 h postischemia and remained elevated for 7 days postinjury. Bax mRNA and bax protein were colocalized to regenerating proximal tubules postischemia and were prominently expressed in papillary proliferations. We conclude that the expressions of bcl-2 and bax in kidney are enhanced in a predictable pattern following acute ischemic injury. Our findings suggest that these regulators of apoptosis play key roles in the process of repair of the damaged proximal tubule postischemia.


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