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Titolo:
Cutting edge: Combined treatment of TNF-alpha and IFN-gamma causes redistribution of junctional adhesion molecule in human endothelial cells
Autore:
Ozaki, H; Ishii, K; Horiuchi, H; Arai, H; Kawamoto, T; Okawa, K; Iwamatsu, A; Kita, T;
Indirizzi:
Kyoto Univ, Fac Med, Grad Sch Med, Dept Geriatr Med,Sakyo Ku, Kyoto 6068507, Japan Kyoto Univ Kyoto Japan 6068507 eriatr Med,Sakyo Ku, Kyoto 6068507, Japan Kirin Brewery Co Ltd, Cent Labs Key Technol, Yokohama, Kanagawa, Japan Kirin Brewery Co Ltd Yokohama Kanagawa Japan , Yokohama, Kanagawa, Japan
Titolo Testata:
JOURNAL OF IMMUNOLOGY
fascicolo: 2, volume: 163, anno: 1999,
pagine: 553 - 557
SICI:
0022-1767(19990715)163:2<553:CECTOT>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
INTERCELLULAR-JUNCTIONS; PECAM-1 CD31; PROTEIN; TRANSMIGRATION; SUPERFAMILY; EXPRESSION; SURFACE; CLONING;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
18
Recensione:
Indirizzi per estratti:
Indirizzo: Ishii, K Kyoto Univ, Fac Med, Grad Sch Med, Dept Geriatr Med,Sakyo Ku, 54 Kawahara Cho, Kyoto 6068507, Japan Kyoto Univ 54 Kawahara Cho Kyoto Japan 6068507 to 6068507, Japan
Citazione:
H. Ozaki et al., "Cutting edge: Combined treatment of TNF-alpha and IFN-gamma causes redistribution of junctional adhesion molecule in human endothelial cells", J IMMUNOL, 163(2), 1999, pp. 553-557

Abstract

Proinflammatory cytokines such as TNF-alpha and IFN-gamma induce cell adhesion molecules in endothelial cells and promote transmigration of leukocytes across endothelial cells. However, when those two were administered together, leukocyte transmigration paradoxically decreased. We cloned a human and bovine homologue of the junctional adhesion molecule (JAM), a novel molecule at the tight junction, and examined the effects of proinflammatory cytokines on JAM in HUVECs, The combined treatment of TNF-alpha pins IFN-gamma caused a disappearance of JAM from intercellular junctions. However, how cytometry, cell ELISA, and subcellular fractionation analysis demonstrated that the amount of JAM was not reduced. This suggested that JAM changed its distribution in response to proinflammatory cytokines. This redistribution of JAM might be involved in a decrease in transendothelial migration of leukocytes at inflammatory sites.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 20/01/21 alle ore 12:18:41