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Titolo:
ENaC- and CFTR-dependent ion and fluid transport in mammary epithelia
Autore:
Blaug, S; Hybiske, K; Cohn, J; Firestone, GL; Machen, TE; Miller, SS;
Indirizzi:
Univ Calif Berkeley, Dept Mol & Cell Biol, Berkeley, CA 94720 USA Univ Calif Berkeley Berkeley CA USA 94720 ll Biol, Berkeley, CA 94720 USA Univ Calif Berkeley, Sch Optometry, Berkeley, CA 94720 USA Univ Calif Berkeley Berkeley CA USA 94720 tometry, Berkeley, CA 94720 USA Duke Univ, Med Ctr, Dept Med, Durham, NC 27710 USA Duke Univ Durham NC USA 27710 iv, Med Ctr, Dept Med, Durham, NC 27710 USA Duke Univ, Med Ctr, Dept Cell Biol, Durham, NC 27710 USA Duke Univ DurhamNC USA 27710 d Ctr, Dept Cell Biol, Durham, NC 27710 USA
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY
fascicolo: 2, volume: 281, anno: 2001,
pagine: C633 - C648
SICI:
0363-6143(200108)281:2<C633:EACIAF>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
TRANSMEMBRANE CONDUCTANCE REGULATOR; RETINAL-PIGMENT EPITHELIUM; GROSS CYSTIC-DISEASE; BREAST-CANCER RISK; SUBMUCOSAL GLANDS; MILK SECRETION; CHANNEL ENAC; FIBROSIS; CELLS; BIOCHEMISTRY;
Keywords:
amiloride; diphenylamine-2-carboxylate; milk secretion; patch clamp; microelectrodes; electrophysiology; cystic fibrosis; tight junctions; leaky and tight epithelia; epithelial sodium channel; cystic fibrosis transmembrane conductance regulator;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
48
Recensione:
Indirizzi per estratti:
Indirizzo: Miller, SS Univ Calif Berkeley, Dept Mol & Cell Biol, 260 Minor Hall, Berkeley, CA 94720 USA Univ Calif Berkeley 260 Minor Hall Berkeley CA USA 9472020 USA
Citazione:
S. Blaug et al., "ENaC- and CFTR-dependent ion and fluid transport in mammary epithelia", AM J P-CELL, 281(2), 2001, pp. C633-C648

Abstract

Mammary epithelial 31EG4 cells (MEC) were grown as monolayers on filters to analyze the apical membrane mechanisms that help mediate ion and fluid transport across the epithelium. RT-PCR showed the presence of cystic fibrosis transmembrane conductance regulator (CFTR) and epithelial Na+ channel (ENaC) message, and immunomicroscopy showed apical membrane staining for both proteins. CFTR was also localized to the apical membrane of native human mammary duct epithelium. In control conditions, mean values of transepithelial potential (apical-side negative) and resistance (R-T) are -5.9 mV and 829Omega .cm(2), respectively. The apical membrane potential (VA) is -40.7 mV, and the mean ratio of apical to basolateral membrane resistance (R-A/R-B)is 2.8. Apical amiloride hyperpolarized V-A by 19.7 mV and tripled R-A/R-B. A cAMP-elevating cocktail depolarized V-A by 17.6 mV, decreased R-A/R-B by 60%, increased short-circuit current by 6 muA/cm(2), decreased R-T by 155Omega .cm(2), and largely eliminated responses to amiloride. Whole cell patch-clamp measurements demonstrated amiloride-inhibited Na+ currents [linear current-voltage (I-V) relation] and forskolin-stimulated Cl- currents (linear I-V relation). A capacitance probe method showed that in the control state, MEC monolayers either absorbed or secreted fluid (2-4 mul.cm(-2).h(-1)). Fluid secretion was stimulated either by activating CFTR (cAMP) or blocking ENaC (amiloride). These data plus equivalent circuit analysis showed that 1) fluid absorption across MEC is mediated by Na+ transport via apical membrane ENaC, and fluid secretion is mediated, in part, by Cl- transport via apical CFTR; 2) in both cases, appropriate counterions move through tight junctions to maintain electroneutrality; and 3) interactions among CFTR, ENaC, and tight junctions allow MEC to either absorb or secrete fluid and, in situ, may help control luminal [Na+] and [Cl-].

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/03/20 alle ore 10:12:11