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首页> 外文期刊>American Journal of Physiology >Caspase-11 promotes cisplatin-induced renal tubular apoptosis through a caspase-3-dependent pathway
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Caspase-11 promotes cisplatin-induced renal tubular apoptosis through a caspase-3-dependent pathway

机译：Caspase-11通过Caspase-3依赖性途径促进顺铂诱导的肾小管细胞凋亡

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摘要

Renal tubular injury is the hallmark of cisplatin-induced nephrotoxicity. Caspase-11, a member of the caspase family, plays an important role in inflammation and cell death. However, its role in cisplatin-induced renal tubular injury remains unclear. In cisplatin-treated mice, caspase-11 expression was significantly elevated and the expression of caspase-11 was mainly located in renal tubule. Inhibition of caspase-11 by small-interference RNA or its inhibitor wedelolactone attenuated cisplatin-induced renal dysfunction and tubular injury. In cultured primary renal tubular epithelial cells, cisplatin significantly promoted the expression and activation of caspase-11. Inhibition of caspase-11 by small-interference RNA reduced cisplatin-induced cell apoptosis. Overexpression of caspase-11 promoted cell apoptosis by activating the caspase-3-related cell apoptosis. Furthermore, coimmunoprecipilation results showed there was a direct interaction between caspase-11 and caspase-3, and the interaction was enhanced by cisplatin. The fluorescence confocal microscopy results showed that caspase-11 and caspase-3 were colocalized in the cytoplasm of renal tubular epithelial cells. These results demonstrate that caspase-11 plays an important role in cisplatin-induced renal tubular injury. Caspase-11 promotes renal epithelial cell apoptosis by activating the caspase-3-dependent apoptotic pathway. Caspase-11 might be a potential target for therapeutic treatment against cisplatin-induced nephrotoxicity.
机译：肾小管损伤是顺铂诱导的肾毒性的标志。 Caspase-11是Caspase系列的成员，在炎症和细胞死亡中起重要作用。然而，其在顺铂诱导的肾小管损伤中的作用仍不清楚。在顺铂处理的小鼠中，Caspase-11表达明显升高，Caspase-11的表达主要位于肾小管中。通过小干扰RNA或其抑制剂Wedellodone对Caspase-11的抑制减去顺铂诱导的肾功能紊乱和管状损伤。在培养的原发性肾小管上皮细胞中，顺铂显着促进了Caspase-11的表达和活化。小干扰RNA降低了Cisplatin诱导的细胞凋亡的Caspase-11的抑制。通过激活胱天蛋白酶-3相关细胞凋亡，Caspase-11促进细胞凋亡的过度表达。此外，Caspase-11和Caspase-3之间的Cimmunoppilipilation结果显示出存在直接相互作用，并通过顺铂增强相互作用。荧光共聚焦显微镜结果表明，Caspase-11和Caspase-3在肾小管上皮细胞的细胞质中分致钙化。这些结果表明，Caspase-11在顺铂诱导的肾小管损伤中起重要作用。通过激活Caspase-3依赖性凋亡途径，促进肾上皮细胞凋亡。 Caspase-11可能是针对顺铂诱导的肾毒性治疗治疗的潜在目标。

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