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Restoration of ENaC expression by glucocorticoid receptor transfection in human HT-29/B6 colon cells.

Abstract：

:The epithelial sodium channel (ENaC) controls colonic sodium absorption. So far, investigation of ENaC was limited by an unexplained lack of steroid-dependent ENaC expression in cultured intestinal cells, which we aimed to resolve. HT-29/B6 cells constitutively expressed the alpha-ENaC subunit, while beta- and gamma-ENaC subunits could not be detected due to deficient basal as well as corticosteroid-induced transcription. This was due to a lack of expression of both activating and inhibiting isoforms of glucocorticoid receptor (GR-alpha, -beta) and mineralocorticoid receptor. Stable transfection of GR-alpha restored intestine-specific glucocorticoid upregulation of beta- and gamma-ENaC in HT-29/B6 cells, which was followed by intact targeting of ENaC channels to the apical cell membrane and dose-dependent induction of electrogenic sodium absorption. In conclusion, ENaC deficiency is due to a lack of steroid receptors and not the consequence of a crypt-like phenotype of cultured intestinal cells. By stable GR transfection we obtained a model, in which ENaC regulation can be studied.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Zeissig S,Fromm A,Mankertz J,Zeitz M,Fromm M,Schulzke JD

doi

10.1016/j.bbrc.2006.04.012

subject

Has Abstract

pub_date

2006-06-16 00:00:00

pages

1065-70

issue

4

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(06)00804-7

journal_volume

344

pub_type

杂志文章

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