Ischemia-induced receptor for activated C kinase (RACK1) expression in rat kidneys

被引:33
作者
Padanilam, BJ
Hammerman, MR
机构
[1] WASHINGTON UNIV, SCH MED, DEPT MED, DIV RENAL, ST LOUIS, MO 63110 USA
[2] WASHINGTON UNIV, SCH MED, DEPT PHYSIOL, DIV RENAL, ST LOUIS, MO 63110 USA
[3] WASHINGTON UNIV, SCH MED, DEPT CELL BIOL, DIV RENAL, ST LOUIS, MO 63110 USA
[4] WASHINGTON UNIV, SCH MED, GEORGE M OBRIEN KIDNEY & UROL DIS CTR, ST LOUIS, MO 63110 USA
关键词
acute renal failure; differential display; polymerase chain reaction;
D O I
10.1152/ajprenal.1997.272.2.F160
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Differential display-polymerase chain reaction (DD-PCR) was used to identify genes that are expressed in kidney following induction of acute ischemic renal injury. The receptor for activated C kinase (RACK1) mRNA expression in kidneys obtained from rats 12 h following ischemia is enhanced twofold compared with 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 enhance the activity of PKC and, in so doing, regulate the process of regeneration of the proximal tubule following ischemic renal injury.
引用
收藏
页码:F160 / F166
页数:7
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