A colonic mineralocorticoid receptor cell model expressing epithelial Na+ channels.

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Bergann T, Ploger S, Fromm A, Zeissig S, Borden SA, Fromm M, Schulzke JD

A colonic mineralocorticoid receptor cell model expressing epithelial Na+ channels.

Biochem Biophys Res Commun. 2009 May 1;382(2):280-5. doi: 10.1016/j.bbrc.2009.03.006. Epub 2009 Mar 9.

PubMed ID

19275887 [ View in PubMed

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Abstract

In the distal colon, the epithelial sodium channel (ENaC) is rate limiting for sodium absorption. Progress in the molecular characterization of ENaC expression and trafficking in response to the mineralocorticoid aldosterone has been hampered, since no epithelial colonic cell line existed expressing functional ENaC stimulated by nanomolar aldosterone via mineralocorticoid receptor (MR). Here, we present a human colonic epithelial cell line inducibly expressing the MR (HT-29/B6-Tet-On-MR) which exhibits aldosterone-dependent ENaC-mediated sodium transport in the presence of the short-chain fatty acid butyrate. Butyrate was necessary for high-level expression of MR which allowed for aldosterone-dependent upregulation of beta- and gamma-ENaC expression. As butyrate alone was not capable of promoting ENaC-mediated sodium transport, aldosterone-induced GILZ (glucocorticoid-induced leucine zipper protein) was identified as a candidate factor increasing apical ENaC levels.

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Drug Targets

Drug	Target	Kind	Organism	Pharmacological Action	Actions
Aldosterone	Mineralocorticoid receptor	Protein	Humans	Unknown	Agonist	Details