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Titolo:
DIFFERENTIAL INDUCTION OF C-FOS, C-JUN, AND APOPTOSIS IN LUNG EPITHELIAL-CELLS EXPOSED TO ROS OR RNS
Autore:
JANSSEN YMW; MATALON S; MOSSMAN BT;
Indirizzi:
UNIV VERMONT,DEPT PATHOL,MED ALUMNI BLDG,RM A-143 BURLINGTON VT 05405 UNIV ALABAMA,DEPT ANESTHESIOL BIRMINGHAM AL 35294
Titolo Testata:
American journal of physiology. Lung cellular and molecular physiology
fascicolo: 4, volume: 17, anno: 1997,
pagine: 789 - 796
SICI:
1040-0605(1997)17:4<789:DIOCCA>2.0.ZU;2-R
Fonte:
ISI
Lingua:
ENG
Soggetto:
NITRIC-OXIDE; PROTOONCOGENE EXPRESSION; NITROGEN-OXIDES; PC12 CELLS; SUPEROXIDE; PROTEIN; ACTIVATION; TRANSCRIPTION; STIMULATION; GENERATION;
Keywords:
NITRIC OXIDE; PEROXYNITRITE; HYDROGEN PEROXIDE; LUNG EPITHELIUM; REACTIVE OXYGEN SPECIES; REACTIVE NITROGEN SPECIES;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
31
Recensione:
Indirizzi per estratti:
Citazione:
Y.M.W. Janssen et al., "DIFFERENTIAL INDUCTION OF C-FOS, C-JUN, AND APOPTOSIS IN LUNG EPITHELIAL-CELLS EXPOSED TO ROS OR RNS", American journal of physiology. Lung cellular and molecular physiology, 17(4), 1997, pp. 789-796

Abstract

Reactive oxygen (ROS) or nitrogen (RNS) species can affect epithelialcells to cause acute damage and an array of pulmonary diseases. The goal of this study was to determine patterns of early response gene expression and functional end points of exposure to nitric oxide (NO .), H2O2, or peroxynitrite (ONOO-) in a line of rat lung epithelial (RLE) cells. Our focus was on c-fos and c-jun protooncogenes, as these genesplay an important role in proliferation or apoptosis, possible end points of exposure to reactive metabolites in lung. Our data demonstratethat NO . generated by spermine 1,3-propanediamine -[1-(3-aminopropyl)-2-hydroxy-2-nitrosohydrazino]- butyl} or S-nitroso-N-acetylpenicillamine as well as H2O2 cause increased c-fos and c-jun mRNA levels, nuclear proteins, and complexes binding the activator protein-1 recognition sequence in RLE cells. These agents also lead to apoptosis and increased membrane permeability. In contrast, exogenously administered ONOO- or 3-morpholinosydnonimine do not induce protooncogenes or apoptosisin RLE cells despite nitration of tyrosines. We conclude that ROS andRNS can elicit distinct molecular and phenotypic responses in a target cell of pulmonary disease.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/11/20 alle ore 09:39:39