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首页> 外文期刊>American Journal of Physiology >Differential subcellular targeting of PKC-epsilon in response to pharmacological or ischemic stimuli in intestinal epithelia.
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Differential subcellular targeting of PKC-epsilon in response to pharmacological or ischemic stimuli in intestinal epithelia.

机译：响应于肠道上皮细胞的药理或缺血性刺激，PKC-ε的亚细胞靶向差异化。

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摘要

Ischemia is the central pathogenic factor underlying a spectrum of intestinal disorders. The study of the cellular signaling responses to ischemic stress in nonepithelial cells has progressed substantially in the previous several years, but little is known about the response in epithelial cells. Unique features of the epithelial response to ischemic stress suggest differential regulation with regards to signaling. The PKC family of proteins has been implicated in ischemic stress in nonepithelial systems. The role of PKC isoforms in chemical ischemia in intestinal epithelial cells is evaluated in this study. Additionally, the phosphorylation of the F-actin cross-linking protein myristoylated alanine-rich C kinase substrate (MARCKS) is also studied. Chemical ischemia resulted in the transient activation of only the isoform PKC-epsilon as detected by translocation employing the subcellular fractionation technique. The pharmacological agonists phorbol 12-myristate 13-acetate and carbachol also led to the translocation of PKC-epsilon. By immunofluoresence, MARCKS is noted to be located at the lateral membrane under control conditions. In response to carbachol, MARCKS translocates to the cytosol, indicating its phosphorylation, which is additionally confirmed biochemically. Consistent with this observation, carbachol induces the translocation of PKC-epsilon to proximity with MARCKS at the lateral membrane. In response to chemical ischemia, MARCKS fails to translocate and phosphorylation does not increase. Additionally, the translocation of PKC-epsilon is not to the lateral membrane but rather basally. The data suggest that the differential translocation of PKC-epsilon in response to pharmacological agonists versus ischemic stress may lead to different effects on downstream targets.
机译：缺血是一系列肠道疾病的主要致病因素。在过去的几年中，对非上皮细胞对缺血性应激的细胞信号转导反应的研究已取得实质性进展，但对上皮细胞的反应知之甚少。上皮对局部缺血应激的反应的独特特征表明信号方面的差异调节。 PKC蛋白家族与非上皮系统的缺血性应激有关。在这项研究中评估了PKC亚型在肠上皮细胞化学缺血中的作用。另外，还研究了F-肌动蛋白交联蛋白肉豆蔻基化的富含丙氨酸的C激酶底物（MARCKS）的磷酸化。化学缺血导致仅亚型PKC-ε的瞬时活化，如通过使用亚细胞分级分离技术进行的转运所检测到的。药理激动剂佛波醇12-肉豆蔻酸酯13-乙酸酯和卡巴胆碱也导致PKC-ε易位。通过免疫荧光，注意到在对照条件下MARCKS位于侧膜。响应于卡巴胆碱，MARCKS易位至胞质溶胶，表明其磷酸化，这在生化上也得到了证实。与该观察结果一致，卡巴胆碱诱导PKC-ε易位至在侧膜处与MARCKS接近。响应化学缺血，MARCKS不能移位，磷酸化不会增加。另外，PKC-ε的易位不是到侧膜，而是基层。数据表明，PKC-ε响应药理激动剂与缺血应激的差异易位可能导致对下游靶点的不同作用。

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