Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Role of E-selectin in bleomycin induced lung fibrosis in mice
Autore:
Azuma, A; Takahashi, S; Nose, M; Araki, K; Araki, M; Takahashi, T; Hirose, M; Kawashima, H; Miyasaka, M; Kudoh, S;
Indirizzi:
Nippon Med Sch, Dept Internal Med 4, Bunkyo Ku, Tokyo 1138602, Japan Nippon Med Sch Tokyo Japan 1138602 ed 4, Bunkyo Ku, Tokyo 1138602, Japan Univ Tsukuba, Inst Basic Med Sci, Tsukuba, Ibaraki 3058575, Japan Univ Tsukuba Tsukuba Ibaraki Japan 3058575 sukuba, Ibaraki 3058575, Japan Ehime Univ, Sch Med, Dept Pathol, Shigenobu, Ehime 7900295, Japan Ehime Univ Shigenobu Ehime Japan 7900295 Shigenobu, Ehime 7900295, Japan Inst Mol Embryol & Genet, Kumamoto 8620976, Japan Inst Mol Embryol & Genet Kumamoto Japan 8620976 Kumamoto 8620976, Japan Kumamoto Univ, Sch Med, Kumamoto 8620976, Japan Kumamoto Univ Kumamoto Japan 8620976 v, Sch Med, Kumamoto 8620976, Japan Kumamoto Univ, Gene Technol Ctr, Kumamoto 8600811, Japan Kumamoto Univ Kumamoto Japan 8600811 echnol Ctr, Kumamoto 8600811, Japan Osaka Univ, Biomed Res Ctr, Sch Med, Dept Bioregulat, Suita, Osaka 5650871, Japan Osaka Univ Suita Osaka Japan 5650871 regulat, Suita, Osaka 5650871, Japan
Titolo Testata:
THORAX
fascicolo: 2, volume: 55, anno: 2000,
pagine: 147 - 152
SICI:
0040-6376(200002)55:2<147:ROEIBI>2.0.ZU;2-R
Fonte:
ISI
Lingua:
ENG
Soggetto:
RESPIRATORY-DISTRESS SYNDROME; INDUCED PULMONARY FIBROSIS; P-SELECTIN; DEFICIENT MICE; LIGAND ESL-1; IN-VIVO; INJURY; EXPRESSION; NEUTROPHILS; BINDING;
Keywords:
E-selectin; sialyl Lewis(x); bleomycin; lung fibrosis;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
38
Recensione:
Indirizzi per estratti:
Indirizzo: Azuma, A Nippon Med Sch, Dept Internal Med 4, Bunkyo Ku, 1-1-5 Sendagi, Tokyo 1138602, Japan Nippon Med Sch 1-1-5 Sendagi Tokyo Japan 1138602 1138602, Japan
Citazione:
A. Azuma et al., "Role of E-selectin in bleomycin induced lung fibrosis in mice", THORAX, 55(2), 2000, pp. 147-152

Abstract

Background-Bleomycin (BLM), a well known anti-cancer drug, often causes acute lung injury and fibrosis by mechanisms that are not well understood. Itis suspected that some proteases and active oxygen species generated from inflammatory cells cause the lung injury and subsequent lung fibrosis. It was therefore hypothesised that inhibition of adhesion of inflammatory cellsto the endothelium might prevent these developments. Methods-BLM (100 mg/kg) was injected into the tail veins of ICR mice to evaluate the induction of E-selectin, an adhesion molecule known to induce neutrophil attachment on endothelial cells. E-selectin mRNA induction was detected by reverse transcriptase polymerase chain reaction (RT-PCR). The myeloperoxidase (MPO) activities in the lung tissues of BLM treated and controlmice were compared to evaluate neutrophil infiltration. Pathological changes in the lungs of soluble E-selectin transgenic mice (TG) and their TG negative (non-TG) littermates after BLM treatment were also compared. Serum samples of TG mice and non-TG mice were tested for their ability to block thebinding of sialyl Lewis(x) to recombinant E-selectin in vitro. Results-E-selectin mRNA was maximally induced at six hours after BLM treatment in the ICR mice. The soluble form of E-selectin which can competitively inhibit the binding of sialylated antigens on inflammatory cells to E- and P-selectins on the endothelium was detected in the serum of TG mice. BLM.induced lung fibrosis occurred in non-TG mice but not in TG mice. This result confirms the finding that the serum of TG mice inhibits the binding of sialyl Lewis(x) to E-selectin in vitro. Conclusion-E-selectin plays an essential role in BLM induced lung fibrosisthrough the induction of neutrophil and other inflammatory cell accumulation, and soluble E-selectin may be of use in the prophylactic treatment of lung fibrosis.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 14/07/20 alle ore 10:38:35