Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
ET-1 stimulates pulmonary arterial smooth muscle cell proliferation via induction of reactive oxygen species
Autore:
Wedgwood, S; Dettman, RW; Black, SM;
Indirizzi:
Northwestern Univ, Sch Med, Dept Pediat, Div Neonatol, Chicago, IL 60611 USA Northwestern Univ Chicago IL USA 60611 iv Neonatol, Chicago, IL 60611 USA Northwestern Univ, Sch Med, Dept Mol Pharmacol, Chicago, IL 60611 USA Northwestern Univ Chicago IL USA 60611 l Pharmacol, Chicago, IL 60611 USA
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
fascicolo: 5, volume: 281, anno: 2001,
pagine: L1058 - L1067
SICI:
1040-0605(200111)281:5<L1058:ESPASM>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
SUPEROXIDE ANION PRODUCTION; NITRIC-OXIDE; ENDOTHELIAL-CELLS; RECEPTOR BLOCKADE; DUCTUS-ARTERIOSUS; NEWBORN-INFANTS; NAD(P)H OXIDASE; GROWTH-FACTORS; FETAL LAMBS; HYPERTENSION;
Keywords:
endothelin-1; free radicals; mitogenesis; hypertension; apoptosis;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
43
Recensione:
Indirizzi per estratti:
Indirizzo: Black, SM Northwestern Univ, Sch Med, Dept Pediat, Div Neonatol, Ward 12-191,303 E Chicago Ave, Chicago, IL 60611 USA Northwestern Univ Ward 12-191,303 E Chicago Ave Chicago IL USA 60611
Citazione:
S. Wedgwood et al., "ET-1 stimulates pulmonary arterial smooth muscle cell proliferation via induction of reactive oxygen species", AM J P-LUNG, 281(5), 2001, pp. L1058-L1067

Abstract

Recent studies implicate reactive oxygen species (ROS) such as superoxide anions and H2O2 in the proliferation of systemic vascular smooth muscle cells (SMCs). However, the role of ROS in SMC proliferation within the pulmonary circulation remains unclear. We investigated the effects of endothelin-1(ET-1), a potential SMC mitogen, on ROS production and proliferation of fetal pulmonary artery SMCs (FPASMCs). Exposure to ET-1 resulted in increasesin superoxide production and viable FPASMCs after 72 h. These increases were prevented by pretreatment with PD-156707. Treatment with pertussis toxinblocked the effects of ET-1, whereas cholera toxin stimulated superoxide production and increased viable cell numbers even in the absence of ET-1. Wortmannin, LY-294002, diphenyleneiodonium (DPI), 4-(2-aminoethyl) benzenesulfonyl fluoride, and apocynin also prevented the ET-1-mediated increases in superoxide production and viable cell numbers. Exposure to H2O2 or diethyldithiocarbamate increased viable cell number by 37% and 50%, respectively. Conversely, ascorbic acid and DPI decreased viable cell number, which appeared to be due to an increase in programmed cell death. Our data suggest thatET-1 exerts a mitogenic effect on FPASMCs via an increase in ROS production and that antioxidants can block this effect via induction of apoptosis. Antioxidant treatment may therefore represent a potential therapy for pulmonary vascular diseases.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/09/20 alle ore 22:50:25