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Titolo:
Na+ transport in normal and CF human bronchial epithelial cells is inhibited by BAY 39-9437
Autore:
Bridges, RJ; Newton, BB; Pilewski, JM; Devor, DC; Poll, CT; Hall, RL;
Indirizzi:
Univ Pittsburgh, Dept Cell Biol & Physiol, Pittsburgh, PA 15261 USA Univ Pittsburgh Pittsburgh PA USA 15261 Physiol, Pittsburgh, PA 15261 USA Bayer Pharmaceut Div, Slough SL2 4LY, Berks, England Bayer Pharmaceut DivSlough Berks England SL2 4LY SL2 4LY, Berks, England
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
fascicolo: 1, volume: 281, anno: 2001,
pagine: L16 - L23
SICI:
1040-0605(200107)281:1<L16:NTINAC>2.0.ZU;2-0
Fonte:
ISI
Lingua:
ENG
Soggetto:
SERINE-PROTEASE INHIBITOR; FIBROSIS LUNG-DISEASE; CYSTIC-FIBROSIS; SODIUM-CHANNEL; PSEUDOHYPOALDOSTERONISM TYPE-1; RESPIRATORY EPITHELIA; AEROSOLIZED AMILORIDE; MUCOCILIARY CLEARANCE; POTENTIAL DIFFERENCE; NEBULIZED AMILORIDE;
Keywords:
cystic fibrosis; Kunitz-type serine protease inhibitor; channel-activating protease; short-circuit current; primary cultures; epithelial sodium channel;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
33
Recensione:
Indirizzi per estratti:
Indirizzo: Bridges, RJ Univ Pittsburgh, Dept Cell Biol & Physiol, 3500 Terrace St,S310 Biomed SciTower, Pittsburgh, PA 15261 USA Univ Pittsburgh 3500 Terrace St,S310 Biomed Sci Tower Pittsburgh PA USA 15261
Citazione:
R.J. Bridges et al., "Na+ transport in normal and CF human bronchial epithelial cells is inhibited by BAY 39-9437", AM J P-LUNG, 281(1), 2001, pp. L16-L23

Abstract

To test the hypothesis that Na+ transport in human bronchial epithelial (HBE) cells is regulated by a protease-mediated mechanism, we investigated the effects of BAY 39-9437, a recombinant Kunitz-type serine protease inhibitor, on amiloride-sensitive short-circuit current of normal [non-cystic fibrosis (CF) cells] and CF HBE cells. Mucosal treatment of non-CF and CF HBE cells with BAY 39-9437 decreased the short-circuit current, with a half-lifeof similar to 45 min. At 90 min, BAY 39-9437 (470 nM) reduced Na+ transport by similar to 70%. The inhibitory effect of BAY 39-9437 was concentrationdependent, with a half-maximal inhibitory concentration of similar to 25 nM. Nai transport was restored to control levels, with a half-life of similar to 15 min, on washout of BAY 39-9437. In addition, trypsin (1 muM) rapidly reversed the inhibitory effect of BAY 39-9437. These data indicate that Na+ transport in HBE cells is activated by a BAY 39-9437-inhibitable, endogenously expressed serine protease. BAY 39-9437 inhibition of this serine protease maybe of therapeutic potential for the treatment of Na+ hyperabsorption in CF.

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Documento generato il 02/10/20 alle ore 01:54:08