• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>American Journal of Physiology >Heat shock prevents simulated ischemia-induced apoptosis in renal tubular cells via a PKC-dependent mechanism.
【24h】

Heat shock prevents simulated ischemia-induced apoptosis in renal tubular cells via a PKC-dependent mechanism.

机译：热休克可通过PKC依赖性机制阻止模拟缺血诱导的肾小管细胞凋亡。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Heat shock produces cellular tolerance to a variety of adverse conditions; however, the protective effect of heat shock on renal cell ischemic injury remains unclear. Protein kinase C (PKC) has been implicated in the signaling mechanisms of acute preconditioning, yet it remains unknown whether PKC mediates heat shock-induced delayed preconditioning in renal cells. To study this, renal tubular cells (LLC-PK1) were exposed to thermal stress (43 degrees C) for 1 h and heat shock protein (HSP) 72 induction was confirmed by Western blot analysis. Cells were subjected to simulated ischemia 24 h after thermal stress, and the effect of heat shock (delayed preconditioning) on ischemia-induced apoptosis (terminal deoxynucleotidyl transferase dUTP nick-end labeling) and B cell lymphoma 2 (Bcl(2)) expression (Western) was determined. Subsequently, the effect of PKC inhibition on HSP72 induction and heat stress-induced ischemic tolerance was evaluated. Thermal stress induced HSP72 production, increased Bcl(2) expression, and prevented simulated ischemia-induced renal tubular cell apoptosis. PKC inhibition abolished thermal induction of HSP72 and prevented heat stress-induced ischemic tolerance. These data demonstrate that thermal stress protects renal tubular cells from simulated ischemia-induced apoptosis through a PKC-dependent mechanism.
机译：热休克产生细胞对多种不利条件的耐受性;然而，热休克对肾细胞缺血性损伤的保护作用仍不清楚。蛋白激酶C（PKC）与急性预适应的信号传导机制有关，但PKC是否介导热休克诱导的肾细胞延迟预适应尚不清楚。为了研究这一点，将肾小管细胞（LLC-PK1）暴露于热应激（43摄氏度）1小时，并通过Western blot分析确认了热休克蛋白（HSP）72的诱导。热应激后24小时对细胞进行模拟缺血，热休克（延迟预处理）对缺血诱导的凋亡（末端脱氧核苷酸转移酶dUTP缺口末端标记）和B细胞淋巴瘤2（Bcl（2））表达的影响（西方）已确定。随后，评估了PKC抑制对HSP72诱导和热应激诱导的缺血耐受的影响。热应激诱导HSP72的产生，增加Bcl（2）的表达，并防止模拟缺血诱导肾小管细胞凋亡。 PKC抑制消除了HSP72的热诱导，并阻止了热应激诱导的缺血耐受。这些数据表明热应激通过PKC依赖性机制保护肾小管细胞免受模拟缺血诱导的凋亡的影响。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号