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Titolo:
BLOOD-RETINAL BARRIER (BRB) BREAKDOWN IN EXPERIMENTAL AUTOIMMUNE UVEORETINITIS - COMPARISON WITH VASCULAR ENDOTHELIAL GROWTH-FACTOR, TUMOR-NECROSIS-FACTOR-ALPHA, AND INTERLEUKIN-1-BETA-MEDIATED BREAKDOWN
Autore:
LUNA JD; CHAN CC; DEREVJANIK NL; MAHLOW J; CHIU C; PENG B; TOBE T; CAMPOCHIARO PA; VINORES SA;
Indirizzi:
JOHNS HOPKINS UNIV,SCH MED,WILMER OPHTHALMOL INST,825 MAUMENEE,600 N WOLFE ST BALTIMORE MD 21287 JOHNS HOPKINS UNIV,SCH MED,WILMER OPHTHALMOL INST BALTIMORE MD 21287 NEI,IMMUNOL LAB,NIH BETHESDA MD 20892
Titolo Testata:
Journal of neuroscience research
fascicolo: 3, volume: 49, anno: 1997,
pagine: 268 - 280
SICI:
0360-4012(1997)49:3<268:BB(BIE>2.0.ZU;2-9
Fonte:
ISI
Lingua:
ENG
Soggetto:
ENDOTOXIN-INDUCED UVEITIS; PERMEABILITY FACTOR; LEWIS RATS; INTRAOCULAR INFLAMMATION; IMMUNOHISTOCHEMICAL LOCALIZATION; ULTRASTRUCTURAL PATHOLOGY; FACTOR EXPRESSION; ALDOSE REDUCTASE; GENE-EXPRESSION; TIGHT JUNCTIONS;
Keywords:
AUTOIMMUNE DISEASE; GROWTH FACTORS; INFLAMMATORY MEDIATORS; CYCLOSPORINE; DEXAMETHASONE; THROMBOXANE SYNTHETASE; VESICULAR TRANSPORT;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
83
Recensione:
Indirizzi per estratti:
Citazione:
J.D. Luna et al., "BLOOD-RETINAL BARRIER (BRB) BREAKDOWN IN EXPERIMENTAL AUTOIMMUNE UVEORETINITIS - COMPARISON WITH VASCULAR ENDOTHELIAL GROWTH-FACTOR, TUMOR-NECROSIS-FACTOR-ALPHA, AND INTERLEUKIN-1-BETA-MEDIATED BREAKDOWN", Journal of neuroscience research, 49(3), 1997, pp. 268-280

Abstract

Experimental autoimmune uveoretinitis (EAU) induced in Lewis rats by immunization with S-antigen is a model of human uveitis. By using immunocytochemical staining for albumin, relatively minor blood-retinal barrier (BRB) breakdown was initially shown in the peripheral retina 8 days after immunization and in the posterior retina by 10 days, Albuminextravasation appeared to occur by opening of the retinal vascular endothelial (RVE) and the retinal pigmented epithelial (RPE) tight junctions, by transendothelial vesicular transport, and by permeating damaged RVE cells. Each of three anti-inflammatory agents reduced or delayed autoimmune-mediated cell destruction but did not eliminate any particular route of extravasation. Vascular endothelial growth factor (VEGF), tumor necrosis factor alpha (TNF alpha), and interleukin-1(beta) (IL-1(beta)) are intimately associated with the development of EAU and are capable of causing BRB dysfunction, A high percentage of RVE tight junctions appeared open ultrastructurally after intravitreal injectionof VEGF (26.7%), TNF alpha (35.6%), or IL-1(beta) (22.1%) compared with saline-injected control (11.4%) or normal, untreated rabbits (4.1%), Heat treatment abolished the effect of IL-1(beta) an the BRB but only partially reduced the effect of VEGF. By 24 hr after injection, the effect of TNF alpha had reversed, but: that of IL-1(beta) had not; VEGF-mediated BRB dysfunction was partially reversible, In addition, albumin-filled vesicle-like structures were seen in the RVE cytoplasm following treatment with each mediator. This study shows that VEGF, TNF alpha, and IL-1(beta) each cause BRB breakdown by opening tight junctions between RVE cells and possibly by increasing transendothelial vesicular transport. Each of these agents may contribute to BRB breakdown inEAU and in patients with uveitis, (C) 1997 Wiley-Liss, Inc.

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Documento generato il 02/12/20 alle ore 04:45:24