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Differential expression of heat shock proteins 70-1 and 70-2 mRNA after ischemia-reperfusion injury of rat kidney.

机译:大鼠肾脏缺血再灌注损伤后热休克蛋白70-1和70-2 mRNA的差异表达

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Ischemia-reperfusion injury in the kidney is known to cause induction of the inducible form of the 70 kDa heat shock protein HSP70i (or HSP72). However, knowledge of the expressional regulation of the two coding genes for HSP70i - HSP70-1 gene and HSP70-2 gene - is very limited. We investigated the time course of HSP70-1 and -2 mRNA expression and its relation to cellular ATP levels in the renal cortex after different periods of unilateral warm renal ischemia (10-60 min) and reperfusion (up to 60 min) in 10-week-old male Wistar rats. Immediately after ischemia there was a significant induction of both HSP70i genes. While HSP70-1 expression constantly increased (up to 4-fold) during reperfusion, even to a higher extent with prolongation of ischemia, HSP70-2 mRNA - which was generally expressed at a far lower level than HSP70-1 mRNA - was strongly induced (3-fold) during reperfusion only after brief periods (10 min) of ischemia. Cellular ATP levels rapidly dropped to 5% with ischemia and the pattern of recovery during reperfusion significantly depended on the duration of the ischemic period, thus showing a good relation with the heat shock (protein) gene expression. We conclude that HSP70-2 is the more sensitive gene with a lower activation threshold by mild injury, while the HSP70-1 gene mediates the major response of heat shock protein induction after severe injury.
机译:已知肾脏的缺血再灌注损伤会引起可诱导形式的70 kDa热休克蛋白HSP70i(或HSP72)的诱导。但是,关于HSP70i的两个编码基因-HSP70-1基因和HSP70-2基因的表达调控的知识非常有限。我们调查了10-60分钟的单侧暖肾缺血(10-60分钟)和再灌注(长达60分钟)不同时期后,肾皮质中HSP70-1和-2 mRNA表达的时程及其与细胞ATP水平的关系。周龄的雄性Wistar大鼠。缺血后立即立即诱导出两种HSP70i基因。尽管HSP70-1的表达在再灌注过程中不断增加(最多4倍),甚至随着缺血时间的延长而增加,但强烈诱导了HSP70-2 mRNA的表达(通常其表达水平远低于HSP70-1 mRNA)。 (3倍)在短暂缺血(10分钟)后再灌注期间。细胞ATP水平随缺血而迅速下降至5%,并且在再灌注期间的恢复模式显着取决于缺血期的持续时间,因此与热休克(蛋白质)基因表达呈良好关系。我们得出的结论是,HSP70-2是较敏感的基因,受轻度损伤的激活阈值较低,而HSP70-1基因介导了严重损伤后热休克蛋白诱导的主要反应。

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