Thyroid hormone potentiates glucocorticoid‐evoked airway Na +  transport without affecting α‐ENaC transcription | Zendy

Richard K. | Zendy; Ramminger S.J. | Zendy; Forsyth L. | Zendy; Burchell A. | Zendy; Wilson S.M. | Zendy

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Thyroid hormone potentiates glucocorticoid‐evoked airway Na + transport without affecting α‐ENaC transcription

Author(s) -

Richard K.,

Ramminger S.J.,

Forsyth L.,

Burchell A.,

Wilson S.M.

Publication year - 2004

Publication title -

febs letters

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.593

H-Index - 257

eISSN - 1873-3468

pISSN - 0014-5793

DOI - 10.1016/j.febslet.2004.09.030

Subject(s) - epithelial sodium channel , glucocorticoid , dexamethasone , hormone , thyroid , endocrinology , medicine , transcription (linguistics) , chemistry , transcription factor , respiratory tract , biology , respiratory system , sodium , gene , biochemistry , linguistics , philosophy , organic chemistry

Glucocorticoid and thyroid hormones (T 3 ) are important for the development of the lungs' Na + absorbing phenotype, which is essential for the integrated functioning of the respiratory tract. Electrometric studies of H441 airway epithelial cells confirmed that dexamethasone increases apical Na + conductance ( G Na ) and demonstrated that T 3 facilitates this control over G Na . Assays of transcriptional activity showed that dexamethasone caused concentration‐dependent activation of the human α‐ENaC promoter (EC 50 ∼5 nM) but, despite its clear effect on G Na , T 3 had no effect upon the transcriptional response to dexamethasone. The facilitation of Na + transport may thus reflect control over events downstream to transcription.

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