Ischemia-induced receptor for activated c kinase (rack1) expression
in rat kidneys.
Padanilam, Babu J., and Marc R. Hammerman.
George M. O'Brien Kidney and Urological Diseases Center, Renal
Division, Departments of Medicine and Cell Biology and Physiology,
Washington University School of Medicine, St. Louis MO 63110
APStracts 3:0192F, 1996.
Differential display polymerase chain reaction (DD-PCR) was used to
identify genes that are expressed in kidney following induction of
acute ischemic renal injury. RACK1 mRNA expression in kidneys
obtained from rats 12 hours following ischemia is enhanced 2-fold
compared to sham-operated rats. The maximal enhancement of expression
(3.3 fold) is at 7 days following reperfusion. Expression remains
elevated at 14 days. RACK1 transcripts and protein are localized to
the damaged and regenerating segments of proximal tubules. At 1 day
following injury, RACK1 protein is present in the epithelial cells of
the damaged S3 segment and in cells sloughed into the tubular lumen.
By 5 days following injury, RACK1 protein expression is enhanced in
the regenerating cells relining the injured tubules of the S3 segment
and in papillary proliferations within regenerating tubules.
Increased expression of RACK1 could enhanced the activity of PKC and
in so doing, regulate the process of regeneration of the proximal
tubule following ischemic renal injury .
Received 22 July 1996; accepted in final form 17 October 1996.
APS Manuscript Number F209-6.
Article publication pending Am. J. Physiol. (Renal Fluid Electrolyte
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 5 November 1996