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首页> 外文期刊>Cellular Physiology and Biochemistry >Control of ion transport in mouse proximal and distal colon by prolactin
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Control of ion transport in mouse proximal and distal colon by prolactin

机译：催乳素控制小鼠近端和远端结肠中的离子迁移

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摘要

The lactogenic hormone prolactin (PRL) has been known to affect Ca2+ and electrolyte transport in the intestinal epithelium. In the present study we analyzed ion transport in mouse proximal and distal colon, and acute changes induced by PRL. In the proximal colon, carbachol activated a Ca2+ dependent Cl- secretion that was sensitive to DIDS and NFA. In the distal colon, both ATP and carbachol activated K+ secretion. Ca2+ - activated KCl transport in proximal and distal colon was inhibited by PRL (200ng/ml), while amiloride sensitive Na+ absorption and cAMP induced Cl- secretion remained unaffected. Luminal large conductance Ca2+-activated K+ (BK) channels were largely responsible for Ca2+-activated K+ secretion in the distal colon, and basolateral BK channels supported Ca2+-activated Cl- secretion in the proximal colon. Ca2+ chelating by BAPTA-AM attenuated effects of carbachol and abolished effects of PRL. Both inhibition of PI3 kinase with wortmannin and blockage of MAP kinases with SB 203580 or U 0126, interfered with the acute inhibitory effect of PRL on ion transport, while blocking of Jak/Stat kinases with AG 490 was without effects. PRL attenuated the increase in intracellular Ca2+ that was caused by stimulation of isolated colonic crypts with carbachol. Thus PRL inhibits Ca2+ dependent Cl- and K+ secretion by interfering with intracellular Ca2+ signaling and probably by activating PI3 kinase and MAP kinase pathways. Copyright (c) 2007 S. Karger AG, Basel.
机译：已知催乳激素催乳激素（PRL）会影响肠上皮中的Ca2 +和电解质运输。在本研究中，我们分析了小鼠近端和远端结肠中的离子转运以及PRL引起的急性变化。在近端结肠中，卡巴胆碱激活了对DIDS和NFA敏感的Ca2 +依赖性Cl-分泌。在远端结肠中，ATP和卡巴胆碱均激活K +分泌。 Ca2 +激活的KCl在近端和远端结肠中的转运受到PRL（200ng / ml）的抑制，而阿米洛利敏感的Na +吸收和cAMP诱导的Cl分泌仍然不受影响。夜光大电导Ca2 +激活的K +（BK）通道主要负责远端结肠中Ca2 +激活的K +分泌，而基底外侧BK通道支持近端结肠中的Ca2 +激活的Cl-分泌。通过BAPTA-AM进行的Ca2 +螯合可减弱卡巴胆碱的作用，并消除PRL的作用。用渥曼青霉素抑制PI3激酶和用SB 203580或U 0126阻断MAP激酶均会干扰PRL对离子转运的急性抑制作用，而用AG 490阻断Jak / Stat激酶则没有作用。 PRL减弱了由卡巴胆碱刺激离体结肠隐窝引起的细胞内Ca2 +的增加。因此，PRL通过干扰细胞内Ca2 +信号传导并可能通过激活PI3激酶和MAP激酶途径来抑制Ca2 +依赖性Cl-和K +分泌。版权所有（c）2007 S.Karger AG，巴塞尔。

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