改变Na +条目对表达的影响基底的顶端和运输蛋白A6上皮细胞。

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Lebowitz J, B,埃丁格RS, Zeidel ML,约翰逊JP

改变Na +条目对表达的影响基底的顶端和运输蛋白A6上皮细胞。

杂志肾杂志。2003年9月,285 (3):F524-31。2003年5月13日Epub。

PubMed ID

12746257 (在PubMed

]

文摘

在几个体内设置,长期改变的速度进入上皮细胞顶端Na +改变这些细胞重吸收钠+的能力。我们以前建模这个负载运输依赖A6细胞通过减少Na +条目通过顶端Na +取消或阿米洛利或加强入境Na +慢性短路(Rokaw医学博士Sarac E, Lechman E,西方M, Angeski J,约翰逊JP,和Zeidel毫升。是杂志细胞杂志270:C600-C607, 1996)。抑制Na +条目通过方法的差别与惊人的对这些运输率以短路电流(Isc)来衡量,而恢复到基底的水平运输在一段时间。相反,upregulation Na +条目的短路导致运输速度持续增加,也回到了基底的水平在一段时间。当前开展的研究来确定是否与这些条件改变整个细胞内容或顶端膜钠离子通道分布(钠)子单元基底或表达式的子单元的Na + - k + atp酶。我们比较这些影响对那些通过长期upregulation Na +运输醛固酮。完整的细胞水平的博后用免疫印迹检测单元18-h抑制Na +条目通过tetramethylammonium更换Na +或顶端阿米洛利或之后18-h增加Na +条目通过慢性短路。这些演习显著改变整个细胞的任何内容博子单元与控制单元。然后我们检查这些演习在顶端膜钠的影响表达式使用领域特定的生物素酰化和免疫印迹。抑制Na +条目通过方法与深刻的顶端膜减少beta-ENaC没有显著变化,顶端膜α或gamma-ENaC数额。 Restoration of apical Na+ and/or removal of amiloride resulted in return of Isc to control levels over 2 h and coincided with return of apical beta-ENaC to control levels without change in apical alpha- or gamma-ENaC. Stimulation of Na+ transport by short-circuiting, in contrast, did not significantly alter apical membrane composition of any of the ENaC subunits. Basolateral expression of Na+-K+-ATPase was also measured by biotinylation and immunoblot and was unchanged under all conditions. Aldosterone increased basolateral expression of the alpha-subunit of Na+-K+-ATPase. These results suggest that chronic downregulation of transport is mediated, in part, by a selective decrease in apical membrane ENaC expression, consistent with our previous observations of noncoordinate regulation of ENaC expression under varying transport conditions in A6 cells. The chronic increase in the rate of Na+ entry is not associated with any of the changes in transporter density at either apical or basolateral membrane seen with aldosterone, suggesting that these two mechanisms of augmenting transport are completely distinct.

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药物靶点

药物	目标	类	生物	药理作用	行动
阿米洛利	Amiloride-sensitive钠离子通道亚基β	蛋白质	人类	是的	抑制剂	细节