Ischemia-induced receptor for activated C kinase (RACK1) expression in rat kidneys.
Ischemia-induced receptor for activated C kinase (RACK1) expression in rat kidneys.
复制标题
大鼠肾脏中缺血诱导的活化 C 激酶受体 (RACK1) 表达。
DOI：
10.1152/ajprenal.1997.272.2.f160
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发表时间：
1997
期刊：
影响因子：
--
通讯作者：
Hammerman,MR
中科院分区：
文献类型：
--
作者：
Padanilam,BJ;Hammerman,MR
差异显示聚合酶链反应（DD-PCR）用于鉴定急性缺血性肾损伤诱导后肾脏中表达的基因。缺血后12 h大鼠肾脏中活化C激酶受体（RACK1） mRNA的表达比假手术大鼠增加了两倍。再灌注后第7天表达增强最大（3.3倍）。在第14天，表达仍然升高。RACK1转录本和蛋白定位于近端小管的受损和再生段。损伤后1天，RACK1蛋白存在于受损S3节段的上皮细胞和脱落到管腔的细胞中。损伤后5天，RACK1蛋白在S3段损伤小管周围的再生细胞和再生小管内的乳头状增生中表达增强。RACK1表达的增加可以增强PKC的活性，从而调节缺血性肾损伤后近端小管的再生过程。
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.