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Titolo:
Prostaglandin E-2 inhibits fibroblast chemotaxis
Autore:
Kohyama, T; Ertl, RF; Valenti, V; Spurzem, J; Kawamoto, M; Nakamura, Y; Veys, T; Allegra, L; Romberger, D; Rennard, SI;
Indirizzi:
Univ Nebraska, Med Ctr, Pulm & Crit Care Med Sect, Omaha, NE 68198 USA Univ Nebraska Omaha NE USA 68198 Crit Care Med Sect, Omaha, NE 68198 USA Vet Affairs Med Ctr, Omaha, NE 68105 USA Vet Affairs Med Ctr Omaha NE USA68105 fairs Med Ctr, Omaha, NE 68105 USA Univ Milan, I-20122 Milan, Italy Univ Milan Milan Italy I-20122Univ Milan, I-20122 Milan, Italy Nippon Med Coll, Dept Pathol 1, Tokyo 1130022, Japan Nippon Med Coll Tokyo Japan 1130022 Dept Pathol 1, Tokyo 1130022, Japan Univ Tokushima, Dept Internal Med 3, Tokushima 7708503, Japan Univ Tokushima Tokushima Japan 7708503 l Med 3, Tokushima 7708503, Japan
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
fascicolo: 5, volume: 281, anno: 2001,
pagine: L1257 - L1263
SICI:
1040-0605(200111)281:5<L1257:PEIFC>2.0.ZU;2-8
Fonte:
ISI
Lingua:
ENG
Soggetto:
BRONCHIAL EPITHELIAL-CELLS; BRONCHOALVEOLAR LAVAGE FLUID; NECROSIS-FACTOR-ALPHA; GROWTH-FACTOR-BETA; LUNG FIBROBLASTS; SUBEPITHELIAL FIBROSIS; FIBRONECTIN PRODUCTION; COLLAGEN; IDENTIFICATION; CONTRACTION;
Keywords:
eicosanoids; adenosine 3 ',5 '-cyclic monophosphate; fibronectin; fibrosis; repair;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
28
Recensione:
Indirizzi per estratti:
Indirizzo: Rennard, SI Univ Nebraska, Med Ctr, Pulm & Crit Care Med Sect, 985125 Nebraska Med Ctr, Omaha, NE 68198 USA Univ Nebraska 985125 Nebraska Med Ctr Omaha NE USA 68198 8 USA
Citazione:
T. Kohyama et al., "Prostaglandin E-2 inhibits fibroblast chemotaxis", AM J P-LUNG, 281(5), 2001, pp. L1257-L1263

Abstract

Fibroblasts are the major source of extracellular connective tissue matrix, and the recruitment, accumulation, and stimulation of these cells are thought to play important roles in both normal healing and the development of fibrosis. Prostaglandin E-2 (PGE(2)) can inhibit this process by blocking fibroblast proliferation and collagen production. The aim of this study was to investigate the inhibitory effect of PGE(2) on human plasma fibronectin (hFN)- and bovine bronchial epithelial cell-conditioned medium (BBEC-CM)-induced chemotaxis of human fetal lung fibroblasts (HFL1). Using the Boyden blind well chamber technique, PGE(2) (10(-7) M) inhibited chemotaxis to hFN 40.8 +/- 5.3% (P < 0.05) and to BBEC-CM 49.7 <plus/minus> 11.7% (P < 0.05). Checkerboard analysis demonstrated inhibition of both chemotaxis and chemokinesis. The effect of PGE(2) was concentration dependent, and the inhibitory effect diminished with time. Other agents that increased fibroblast cAMPlevels, including isoproterenol (10(-5) M), dibutyryl cAMP (10(-5) M), andforskolin (3 x 10(-5) M) had similar effects and inhibited chemotaxis 54.1, 95.3, and 87.0%, respectively. The inhibitory effect of PGE(2) on HFL1 cell chemotaxis was inhibited by the cAMP-dependent protein kinase (PKA) inhibitor KT-5720, which suggests a cAMP-dependent effect mediated by PKA. In summary, PGE(2) appears to inhibit fibroblast chemotaxis, perhaps by modulating the rate of fibroblast migration. Such an effect may contribute to regulation of the wound healing response after injury.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 07/04/20 alle ore 22:56:55