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Titolo:
Mechanisms of TNF-alpha stimulation of amiloride-sensitive sodium transport across alveolar epithelium
Autore:
Fukuda, N; Jayr, C; Lazrak, A; Wang, YB; Lucas, R; Matalon, S; Matthay, MA;
Indirizzi:
Univ Calif San Francisco, Cardiovasc Res Inst, San Francisco, CA 94143 USAUniv Calif San Francisco San Francisco CA USA 94143 ancisco, CA 94143 USA Univ Alabama, Dept Anesthesiol Physiol & Biophys, Birmingham, AL 35223 USAUniv Alabama Birmingham AL USA 35223 & Biophys, Birmingham, AL 35223 USA Weizmann Inst Sci, Dept Biol Chem, IL-76100 Rehovot, Israel Weizmann Inst Sci Rehovot Israel IL-76100 Chem, IL-76100 Rehovot, Israel
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
fascicolo: 6, volume: 280, anno: 2001,
pagine: L1258 - L1265
SICI:
1040-0605(200106)280:6<L1258:MOTSOA>2.0.ZU;2-Y
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-NECROSIS-FACTOR; APICAL MEMBRANE-VESICLES; LUNG LIQUID CLEARANCE; G-PROTEINS; MOLECULAR CHARACTERIZATION; BIOELECTRIC PROPERTIES; BIOPHYSICAL PROPERTIES; ANESTHETIZED SHEEP; BARRIER FUNCTION; GENE-EXPRESSION;
Keywords:
tumor necrosis factor-alpha; tumor necrosis factor receptor; patch clamp; alveolar epithelial cell; acute lung injury; pulmonary edema; pneumonia;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
57
Recensione:
Indirizzi per estratti:
Indirizzo: Matthay, MA Univ Calif San Francisco, Cardiovasc Res Inst, 505 Parnassus Ave,HSW-825, San Francisco, CA 94143 USA Univ Calif San Francisco 505 Parnassus Ave,HSW-825 San Francisco CA USA 94143
Citazione:
N. Fukuda et al., "Mechanisms of TNF-alpha stimulation of amiloride-sensitive sodium transport across alveolar epithelium", AM J P-LUNG, 280(6), 2001, pp. L1258-L1265

Abstract

Because tumor necrosis factor (TNF)-alpha can upregulate alveolar fluid clearance (AFC) in pneumonia or septic peritonitis, the mechanisms responsible for the TNF-alpha -mediated increase in epithelial fluid transport were studied. In rats, 5 mug of TNF-alpha in the alveolar instillate increased AFC by 67%. This increase was inhibited by amiloride but not by propranolol. We also tested a triple-mutant TNF-alpha that is deficient in the lectinlike tip portion of the molecule responsible for its membrane conductance effect; the mutant also has decreased binding affinity to both TNF-alpha receptors. The triple-mutant TNF-alpha did not increase AFC. Perfusion of human A549 cells, patched in the whole cell mode, with TNF-alpha (120 ng/ml) resulted in a sustained increase in Na+ currents from 82 +/- 9 to 549 +/- 146 pA(P < 0.005; n = 6). The TNF-<alpha>-elicited Na+ current was inhibited by amiloride, and there was no change when A549 cells were perfused with the triple-mutant TNF-alpha or after preincubation with blocking antibodies to the two TNF-alpha receptors before perfusion with TNF-alpha. In conclusion, although TNF-alpha can initiate acute inflammation and edema formation in the lung, TNF-alpha can also increase AFC by an amiloride-sensitive, cAMP-independent mechanism that enhances the resolution of alveolar edema in pathological conditions by either binding to its receptors or activating Na+ channels by means of its lectinlike domain.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 01/04/20 alle ore 23:34:30