title: Expression of ENaC and serum- and glucocorticoid-induced kinase 1 in the rat intestinal epithelium.
abstract: 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.
authors: Department of Cellular and Molecular Psysiology, Yale University School of Medicine, New Haven, Connecticut 06520-8026, USA.
authors: Tatjana
authors: T
authors: Coric
authors: Nelmary
authors: N
authors: Hernandez
authors: Diego
authors: D
authors: Alvarez de la Rosa
authors: Deren
authors: D
authors: Shao
authors: Tong
authors: T
authors: Wang
authors: Cecilia M
authors: CM
authors: Canessa
mesh_terms: D000450:Aldosterone / Q000494:pharmacology; D000818:Animals; D019138:Antibodies, Blocking / Q000494:pharmacology; D000918:Antibody Specificity; D015152:Blotting, Northern; D016466:CHO Cells; D003106:Colon / Q000187:drug effects / Q000378:metabolism; D006224:Cricetinae; D018076:DNA, Complementary / Q000096:biosynthesis / Q000235:genetics; D004790:Enzyme Induction / Q000187:drug effects; D053503:Epithelial Sodium Channels; D004848:Epithelium / Q000378:metabolism; D005455:Fluorescent Antibody Technique; D017874:Immediate-Early Proteins; D007413:Intestinal Mucosa / Q000201:enzymology / Q000378:metabolism*; D009687:Nuclear Proteins; D010957:Plasmids / Q000235:genetics; D017346:Protein Serine-Threonine Kinases / Q000037:antagonists & inhibitors / Q000096:biosynthesis*; D012333:RNA, Messenger / Q000096:biosynthesis; D051381:Rats; D015398:Signal Transduction / Q000187:drug effects; D015222:Sodium Channels / Q000096:biosynthesis*; D000099184:Serum-Glucocorticoid Regulated Kinases
chemical_list: D000450:Aldosterone; D019138:Antibodies, Blocking; D018076:DNA, Complementary; D053503:Epithelial Sodium Channels; D017874:Immediate-Early Proteins; D009687:Nuclear Proteins; D017346:Protein Serine-Threonine Kinases; D012333:RNA, Messenger; D015222:Sodium Channels; D000099184:Serum-Glucocorticoid Regulated Kinases