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首页> 外文期刊>American Journal of Physiology >Aquaporin-2, a regulated water channel, is expressed in apical membranes of rat distal colon epithelium.
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Aquaporin-2, a regulated water channel, is expressed in apical membranes of rat distal colon epithelium.

机译:Aquaporin-2是一种调节水通道,在大鼠远端结肠上皮的顶膜中表达。

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摘要

Aquaporin-2 (AQP-2) is the vasopressin-regulated water channel expressed in the apical membrane of principal cells in the collecting duct and is involved in the urinary concentrating mechanism. In the rat distal colon, vasopressin stimulates water absorption through an unknown mechanism. With the hypothesis that AQP-2 could contribute to this vasopressin effect, we studied its presence in rat colonic epithelium. We used RT-PCR, in situ hybridization, immunoblotting, and immunocytochemistry to probe for AQP-2 expression. An AQP-2 amplicon was obtained through RT-PCR of colon epithelium RNA, and in situ hybridization revealed AQP-2 mRNA in colonic crypts and, to a lesser extent, in surface absorptive epithelial cells. AQP-2 protein was localized to the apical membrane of surface absorptive epithelial cells, where it colocalized with H(+)-K(+)-ATPase but not with Na(+)-K(+)-ATPase. AQP-2 was absent from the small intestine, stomach, and liver. Water deprivation increased the hybridization signal and the protein level (assessed by Western blot analysis) for AQP-2 in distal colon. This was accompanied by increased p-chloromercuriphenylsulfonic acid-sensitive water absorption. These results indicate that AQP-2 is present in the rat distal colon, where it might be involved in a water-sparing mechanism. In addition, these results support the idea that AQP-2, and probably other aquaporins, are involved in water absorption in the colon.
机译:水通道蛋白2(AQP-2)是血管加压素调节的水通道,在收集管中主细胞的顶膜中表达,并参与尿液浓缩机制。在大鼠远端结肠中,加压素通过未知机制刺激水吸收。假设AQP-2可能有助于这种加压素的作用,我们研究了其在大鼠结肠上皮中的存在。我们使用RT-PCR,原位杂交,免疫印迹和免疫细胞化学来探测AQP-2表达。通过结肠上皮RNA的RT-PCR获得AQP-2扩增子,并且原位杂交揭示了结肠隐窝以及表面吸收性上皮细胞中的AQP-2 mRNA。 AQP-2蛋白定位于表面吸收上皮细胞的顶膜,在这里它与H(+)-K(+)-ATPase共定位,而不与Na(+)-K(+)-ATPase共定位。小肠,胃和肝脏中缺少AQP-2。缺水增加了远端结肠中AQP-2的杂交信号和蛋白质水平(通过蛋白质印迹分析评估)。这伴随着对氯巯基苯基磺酸对水的敏感性增加。这些结果表明,AQP-2存在于大鼠远端结肠中,它可能参与了节水机制。此外,这些结果支持了AQP-2和其他水通道蛋白可能参与结肠吸水的想法。

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