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Titolo:
Effects of endothelin-1 and nitric oxide on proliferation of cultured guinea pig bronchial smooth muscle cells
Autore:
Kizawa, Y; Ohuchi, N; Saito, K; Kusama, T; Murakami, H;
Indirizzi:
Nihon Univ, Coll Pharm, Dept Physiol & Anat, Funabashi, Chiba 2748555, Japan Nihon Univ Funabashi Chiba Japan 2748555 Funabashi, Chiba 2748555, Japan
Titolo Testata:
COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY C-TOXICOLOGY & PHARMACOLOGY
fascicolo: 4, volume: 128, anno: 2001,
pagine: 495 - 501
SICI:
1532-0456(200104)128:4<495:EOEANO>2.0.ZU;2-I
Fonte:
ISI
Lingua:
ENG
Soggetto:
RELAXING FACTOR; ETA-RECEPTOR; ASTHMA; EPITHELIUM; IRL-1620; TRACHEA; CONTRACTIONS; ANTAGONISTS; EXPRESSION; RELAXATION;
Keywords:
endothelin-1; NO; mitogenesis; EGF; SIN-1; ODQ; BQ-123; BQ-788; bronchus; smooth muscle; guinea pig;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
36
Recensione:
Indirizzi per estratti:
Indirizzo: Murakami, H Nihon Univ, Coll Pharm, Dept Physiol & Anat, Funabashi, Chiba 2748555, Japan Nihon Univ Funabashi Chiba Japan 2748555 Chiba 2748555, Japan
Citazione:
Y. Kizawa et al., "Effects of endothelin-1 and nitric oxide on proliferation of cultured guinea pig bronchial smooth muscle cells", COMP BIOC C, 128(4), 2001, pp. 495-501

Abstract

The proliferative effects of endothelin-1 (ET-1), both alone and in combination with epidermal growth factor (EGF), and the effect of nitric oxide (NO) on the cell proliferation were investigated in cultured guinea pig bronchial smooth muscle cells. ET-I (10-100 nM) alone augmented cell proliferation. and was additive to the effect of EGF (0.48 nM) in a concentration-dependent manner. An ETA antagonist, BQ-123 (10 muM) reduced the cell-proliferative effect of ET-I. whereas an ETB antagonist, BQ-788 (10 muM), did not influence the effect. A NO donor, SIN-I (10 nM-1 muM), reduced the cell-proliferative effect of ET-I in a concentration-dependent manner. The effect of SIN-1 (1 muM) was partly, but significantly, reversed by a soluble guanylylcyclase inhibitor, ODQ(1 muM) These results suggest that ET-1 acts not only as a co-mitogen with EGF but also as a mitogen alone, and that its actionis mediated through activation of ETA receptors. Therefore, ET-I may contribute to airway remodeling, a pathophysiological hallmark of asthma. In addition, NO, which is produced mainly in the airway epithelium and is partly mediated through cGMP-dependent pathway, may reduce the phenomenon. (C) 2001 Elsevier Science Inc. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 09/07/20 alle ore 14:02:51