ISCHEMIA-INDUCED RECEPTOR FOR ACTIVATED C-KINASE (RACK1) EXPRESSION IN RAT KIDNEYS

Citation
Bj. Padanilam et Mr. Hammerman, ISCHEMIA-INDUCED RECEPTOR FOR ACTIVATED C-KINASE (RACK1) EXPRESSION IN RAT KIDNEYS, American journal of physiology. Renal, fluid and electrolyte physiology, 41(2), 1997, pp. 160-166
Citations number
19
Categorie Soggetti
Physiology
ISSN journal
03636127
Volume
41
Issue
2
Year of publication
1997
Pages
160 - 166
Database
ISI
SICI code
0363-6127(1997)41:2<160:IRFAC(>2.0.ZU;2-N
Abstract
Differential display-polymerase chain reaction (DD-PCR) was used to id entify genes that are expressed in kidney following induction of acute ischemic renal injury. The receptor for activated C kinase (RACK1) mR NA expression in kidneys obtained from rats 12 h following ischemia is enhanced twofold compared with sham-operated rats. The maximal enhanc ement of expression (3.3-fold) is at 7 days following reperfusion. Exp ression remains elevated at 14 days. RACK1 transcripts and protein are localized to the damaged and regenerating segments of proximal tubule s. At 1 day following injury, RACK1 protein is present in the epitheli al cells of the damaged S3 segment and in cells sloughed into the tubu lar lumen. By 5 days following injury, RACK1 protein expression is enh anced in the regenerating cells relining the injured tubules of the S3 segment and in papillary proliferations within regenerating tubules. Increased expression of RACK1 could enhance the activity of PKC and, i n so doing, regulate the process of regeneration of the proximal tubul e following ischemic renal injury.