Sex and estrous cycle-dependent rapid protein kinase signaling actions of estrogen in distal colonic cells
Sex and estrous cycle-dependent rapid protein kinase signaling actions of estrogen in distal colonic cells
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DOI：
10.1016/j.steroids.2008.01.021
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发表时间：
2008-10-01
期刊：
影响因子：
2.7
通讯作者：
Harvey, Brian J.
中科院分区：
文献类型：
--
作者：
O'Mahony, Fiona;Harvey, Brian J.
本实验室以前的研究表明，17β-雌二醇(E_2)能迅速抑制大鼠和人远端结肠上皮细胞的氯离子分泌。这种抑制作用是通过靶向被确认为KCNQ1(KvLQT1)通道的基侧K+通道发生的。E2通过第二信使的级联间接调节通道的活性，第二信使对E2的反应迅速被磷酸化。其抗分泌机制可能是在高循环血浆E_2期间，E_2导致液体滞留在肠内。在这里，我们回顾了性别依赖和发情周期的调节，这一新的快速反应E2。抑制KCNQ1通道活性和氯离子的分泌，将在未来研究雌激素在女性组织中的滞留作用，并在肠道分泌障碍和药物靶点的研究中具有重要意义。(C)2008 Elsevier Inc.保留所有权利。
Previous studies from our laboratory demonstrated that 17 beta-estradiol (E2) rapidly inhibits Cl- secretion in rat and human distal colonic epithelium. The inhibition has been shown to occur via targeting of a basolateral K+ channel identified as the KCNQ1 (KvLQT1) channel. E2 indirectly modulates the channel activity via a cascade of second messengers which are rapidly phosphorylated in response to E2. The anti-secretory mechanism may be the manner by which E2 induces fluid retention in the intestine during periods of high circulating plasma E2. Here we review the sex-dependent and estrous cycle regulation of this novel rapid response to E2. The inhibition of KCNQ1 channel activity and Cl- secretion will be of interest in the future in the investigation of the retentive effects of estrogen in female tissue and also in the study of secretory disorders and drugable targets of the intestine. (C) 2008 Elsevier Inc. All rights reserved.