Expression of ENaC and serum- and glucocorticoid-induced kinase 1 in the rat intestinal epithelium

被引:36
作者
Coric, T [1 ]
Hernandez, N [1 ]
de la Rosa, DA [1 ]
Shao, D [1 ]
Wang, T [1 ]
Canessa, CM [1 ]
机构
[1] Yale Univ, Sch Med, Dept Cellular & Mol Physiol, New Haven, CT 06520 USA
来源
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY | 2004年 / 286卷 / 04期
关键词
aldosterone; sodium depletion; distal colon; amiloride; serum- and glucocorticoid-induced kinase 1;
D O I
10.1152/ajpgi.00364.2003
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Increase in epithelium sodium channel (ENaC) activity induced by aldosterone in the distal tubule of the kidney has been attributed to serum- and glucocorticoid-induced kinase 1 (sgk1). The distal colon constitutes another classical aldosterone-responsive epithelium that expresses both ENaC and sgk1 in an aldosterone-dependent manner. However, the site of expression and the temporal relationship of the aldosterone induction of these two proteins have not been investigated. Here, we examined the distribution and abundance of sgk1 in the rat intestine under basal conditions and after changes in the concentration of aldosterone and glucocorticoids. Results indicate that sgk1 is expressed in the distal colon and also in the ileum and jejunum. Abundance of sgk1 was high in control animals, and it did not change significantly after sodium depletion or after a single dose of aldosterone; however, it decreased after adrenalectomy. In contrast, the three subunits of ENaC were markedly induced in the distal colon by acute and chronic increases in aldosterone levels. Results indicate differential regulation of sgk and ENaC subunits by aldosterone in the distal colon. Distribution of sgk1 in the intestine beyond the aldosterone-responsive segments suggests that sgk1 may additionally regulate other sodium transporters in the intestinal epithelium.
引用
收藏
页码:G663 / G670
页数:8
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