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Titolo:
The alpha-subunit of the epithelial sodium channel is an aldosterone-induced transcript in mammalian collecting ducts, and this transcriptional response is mediated via distinct cis-elements in the 5 '-flanking region of thegene
Autore:
Mick, VE; Itani, OA; Loftus, RW; Husted, RF; Schmidt, TJ; Thomas, CP;
Indirizzi:
Univ Iowa, Coll Med, Dept Internal Med, Iowa City, IA 52242 USA Univ IowaIowa City IA USA 52242 pt Internal Med, Iowa City, IA 52242 USA Univ Iowa, Coll Med, Dept Physiol & Biophys, Iowa City, IA 52242 USA Univ Iowa Iowa City IA USA 52242 ysiol & Biophys, Iowa City, IA 52242 USA Vet Affairs Med Ctr, Iowa City, IA 52242 USA Vet Affairs Med Ctr Iowa City IA USA 52242 d Ctr, Iowa City, IA 52242 USA
Titolo Testata:
MOLECULAR ENDOCRINOLOGY
fascicolo: 4, volume: 15, anno: 2001,
pagine: 575 - 588
SICI:
0888-8809(200104)15:4<575:TAOTES>2.0.ZU;2-A
Fonte:
ISI
Lingua:
ENG
Soggetto:
SENSITIVE NA+ CHANNEL; RECEPTOR-KNOCKOUT MICE; MINERALOCORTICOID-RECEPTOR; GLUCOCORTICOID RECEPTOR; CELL-LINE; STEROID-HORMONES; XENOPUS OOCYTES; TRANSPORT; EXPRESSION; KIDNEY;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
53
Recensione:
Indirizzi per estratti:
Indirizzo: Thomas, CP Univ Iowa, Coll Med, Dept Internal Med, E300 GH,200 Hawkins Dr,Iowa City,IA 52242 USA Univ Iowa E300 GH,200 Hawkins Dr Iowa City IA USA 52242 242 USA
Citazione:
V.E. Mick et al., "The alpha-subunit of the epithelial sodium channel is an aldosterone-induced transcript in mammalian collecting ducts, and this transcriptional response is mediated via distinct cis-elements in the 5 '-flanking region of thegene", MOL ENDOCR, 15(4), 2001, pp. 575-588

Abstract

Aldosterone stimulates Na+ reabsorption in the collecting ducts by increasing the activity of the epithelial sodium channel, ENaC, Systemic administration of aldosterone increases alpha ENaC mRNA expression in mammalian kidney, suggesting that the alpha ENaC gene is a target for aldosterone action in the distal nephron, To determine whether aldosterone increases alpha ENaC gene transcription, a portion of the alpha ENaC 5'-flanking region coupled to luciferase was transfected into MDCK-C7 cells, a collecting duct cell line with aldosterone-stimulated Na+ transport. Both dexamethasone and aldosterone stimulated alpha ENaC-coupled reporter gene activity via the glucocorticoid receptor (GR), and this response correlated with the effect of these hormones on endogenous alpha ENaC expression. The aldosterone-stimulatedalpha ENaC expression was blocked by actinomycin D, and aldosterone had noeffect on alpha ENaC mRNA decay, confirming a transcriptional effect. In HT-29 cells, a GR/mineralocorticoid receptor (MR)-deficient colonic cell line with constitutive alpha ENaC expression, cotransfection with GR or MR restored aldosterone-stimulated aENaC gene transcription, although aldosteronehad a functional preference for MR. Analysis of deletion constructs confirmed that a single imperfect glucocorticoid response element (GRE) is necessary and sufficient to confer the aldosterone responsiveness to the alpha ENaC gene promoter in MDCK-C7 and HT-29 cells. These results confirm that alpha ENaC is an aldosterone-induced transcript in the collecting duct and delineates the molecular mechanism for this effect.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 21/05/18 alle ore 13:03:50