TRANSIENT ISCHEMIA OR HEAT-STRESS INDUCES A CYTOPROTECTANT PROTEIN IN RAT-KIDNEY

TRANSIENT ISCHEMIA OR HEAT-STRESS INDUCES A CYTOPROTECTANT PROTEIN IN RAT-KIDNEY
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DOI:
10.1152/ajprenal.1991.260.4.f479
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发表时间:
1991-04-01
影响因子:
--
通讯作者:
BORKAN, SC
BORKAN, SC
中科院分区:
其他
文献类型:
--
作者:
EMAMI, A;SCHWARTZ, JH;BORKAN, SC

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亚致死热暴露会诱导包括大鼠肾脏在内的多种组织产生热应激蛋白 (HSP) 72 kDa,这是一种据报道的细胞保护剂。 然而,尚未描述HSP 72响应热或其他细胞应激(例如短暂性缺血)在肾脏中积聚的定位和时间过程。 在暴露于 42 +/- 0.5 摄氏度(热应激)或 37 摄氏度(假手术)15 分钟的麻醉大鼠中,使用特异性单克隆抗 HSP 72 抗体通过免疫印迹分析检测到肾匀浆中 HSP 72 的积累在热应激后 4-6 小时达到峰值,并持续 10 天。 HSP 72 在热应激后 1 小时内迅速出现在肾乳头中,并在 4 小时内出现在髓质和皮质中。 在假热应激的组织中没有检测到 HSP 72。 HSP 72 也在肾原位缺血至少 15 分钟的 3 小时内检测到。 缺血 60 分钟后累积达到最大,并持续 5 天,而缺血 90 分钟后或任何时间点的对侧非缺血肾脏中均未检测到 HSP 72。 这项研究表明,短暂性缺血(如热应激)会导致 HSP 72 快速在细胞质中积累,HSP 72 是一种已知的细胞保护剂,对于介导细胞修复或增强对后续损伤的抵抗力可能很重要。
Sublethal heat exposure induces the production of heat stress protein (HSP) 72 kDa, a reported cytoprotectant, in several tissues including the rat kidney. However, the localization and time course of HSP 72 accumulation in the kidney in response to heat or other cell stresses such as transient ischemia have not been described. In anesthetized rats exposed to either 42 +/- 0.5-degrees-C (heat stress) or 37-degrees-C (sham) for 15 min, accumulation of HSP 72 in kidney homogenates, detected by immunoblot analysis using a specific monoclonal anti-HSP 72 antibody, peaked 4-6 h after heat stress and persisted for 10 days. HSP 72 appeared rapidly in renal papilla within 1 h and in medulla and cortex within 4 h after heat stress. No HSP 72 was detected in tissues from sham heat stress. HSP 72 was also detected within 3 h of at least 15 min of renal ischemia in situ. Accumulation was maximal after 60 min of ischemia and persisted for 5 days, whereas no HSP 72 was detected after 90 min of ischemia or in the contralateral nonischemic kidney at any time point. This study demonstrates that transient ischemia, like heat stress, results in the rapid cytosolic accumulation of HSP 72, a known cytoprotectant that may be important in mediating cell repair or increasing resistance to subsequent injury.