Expression and function of the epithelial sodium channel δ-subunit in human respiratory epithelial cells in vitro.
Expression and function of the epithelial sodium channel δ-subunit in human respiratory epithelial cells in vitro.
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体外人呼吸道上皮细胞上皮钠通道δ亚基的表达和功能。
DOI：
10.1007/s00424-015-1693-5
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发表时间：
2015
期刊：
影响因子：
--
通讯作者：
Ehrhardt,Carsten
中科院分区：
文献类型：
--
作者：
Schwagerus,Elena;Sladek,Svenja;Buckley,StephenT;Armas-Capote,Natalia;AlvarezdelaRosa,Diego;Harvey,BrianJ;Fischer,Horst;Illek,Beate;Huwer,Hanno;Schneider-Daum,Nicole;Lehr,Claus-Michael;Ehrhardt,Carsten
Using human airway epithelial cell lines (i.e. NCI-H441 and Calu-3) as well as human alveolar epithelial type I-like (ATI) cells in primary culture, we studied the contribution of the epithelial sodium channel δ-subunit (δ-ENaC) to transepithelial sodium transport in human lung in vitro. Endogenous δ-ENaC protein was present in all three cell types tested; however, protein abundance was low, and no expression was detected in the apical cell membrane of these cells. Similarly, known modulators of δ-ENaC activity, such as capsazepine and icilin (activators) and Evans blue (inhibitor), did not show effects on short-circuit current (ISC), suggesting that δ-ENaC is not involved in the modulation of transcellular sodium absorption in NCI-H441 cell monolayers. Over-expression of δ-ENaC in NCI-H441 cells resulted in detectable protein expression in the apical cell membrane, as well as capsazepine and icilin-stimulated increases inISCthat were effectively blocked by Evans blue and that were consistent with δ-ENaC activation and inhibition, respectively. Consequently, these observations suggest that δ-ENaC expression is low in NCI-H441, Calu-3, and ATI cells and does not contribute to transepithelial sodium absorption.
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