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首页> 外文期刊>Journal of biochemical and molecular toxicology >Clostridium difficile toxin A and toxin B inhibit YAP in the colonic epithelial cells
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Clostridium difficile toxin A and toxin B inhibit YAP in the colonic epithelial cells

机译：Clostridium艰难梭菌毒素A和毒素B抑制结肠上皮细胞中的YAP

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摘要

Toxin A (TcdA) and toxin B (TcdB), the two exotoxins of Clostridium difficile, are main causal agents for the colonic epithelium damage in Clostridium difficile infection (CDI). The Hippo pathway is crucial for the control of tissue homeostasis and regeneration of intestines. However, the dysregulation of Hippo pathway in CDI is unclear. Here we show that YAP and TAZ, the transcriptional coactivators downstream of the Hippo pathway, are sequestered in the cytoplasm, degraded, and inactivated by treatment with TcdA and TcdB in colonic epithelial cells. The over-expression of YAP restores the messenger RNA expressions of YAP target genes, attenuates the disruption of cytoskeleton and cell rounding, and rescues the cell proliferation of colonic epithelial cells under exposure of the two toxins. Our results demonstrate that inhibition of YAP and TAZ is involved in the pathogenesis of CDI, implicating that increasing YAP activity could be a potential therapeutic strategy for the CDI treatment.
机译：艰难梭菌外毒素A（TcdA）和毒素B（TcdB）是艰难梭菌感染（CDI）时结肠上皮损伤的主要原因。Hippo通路对于控制组织内稳态和肠道再生至关重要。然而，CDI中Hippo通路的失调尚不清楚。在这里，我们发现Hippo途径下游的转录辅激活子YAP和TAZ在结肠上皮细胞中被隔离在细胞质中，被TcdA和TcdB降解并失活。YAP的过度表达恢复了YAP靶基因的信使RNA表达，减轻了细胞骨架和细胞圆整的破坏，并在两种毒素暴露下拯救了结肠上皮细胞的细胞增殖。我们的结果表明，YAP和TAZ的抑制参与了CDI的发病机制，这意味着增加YAP活性可能是CDI治疗的潜在治疗策略。

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