Abstract:
:Aldosterone treatment of M1-CCD cells stimulated an increase in epithelial Na(+) channel (ENaC) alpha-subunit expression that was mainly localized to the apical membrane. PKD1-suppressed cells constitutively expressed ENaCalpha at low abundance, with no increase after aldosterone treatment. In the PKD1-suppressed cells, ENaCalpha was mainly localized proximal to the basolateral surface of the epithelium both before and after aldosterone treatment. Apical membrane insertion of ENaCbeta in response to aldosterone treatment was also sensitive to PKD1 suppression as was the aldosterone-induced rise in the amiloride-sensitive, trans-epithelial current (I(TE)). The interaction of the mineralocorticoid receptor (MR) with specific elements in the promoters of aldosterone responsive genes is stabilized by ligand interaction and phosphorylation. PKD1 suppression inhibited aldosterone-induced SGK-1 expression. The nuclear localization of MR was also blocked by PKD1 suppression and MEK antagonism implicating both these kinases in MR nuclear stabilization. PKD1 thus modulates aldosterone-induced ENaC activity through the modulation of sub-cellular trafficking and the stabilization of MR nuclear localization.
journal_name
Mol Cell Endocrinoljournal_title
Molecular and cellular endocrinologyauthors
McEneaney V,Dooley R,Yusef YR,Keating N,Quinn U,Harvey BJ,Thomas Wdoi
10.1016/j.mce.2010.04.019subject
Has Abstractpub_date
2010-08-30 00:00:00pages
8-17issue
1-2eissn
0303-7207issn
1872-8057pii
S0303-7207(10)00236-4journal_volume
325pub_type
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