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Titolo:
HIV-1 Tat increases endothelial solute permeability through tyrosine kinase and mitogen-activated protein kinase-dependent pathways
Autore:
Oshima, T; Flores, SC; Vaitaitis, G; Coe, LL; Joh, T; Park, JH; Zhu, YN; Alexander, B; Alexander, JS;
Indirizzi:
Webb Waring Inst Biomed Res, Denver, CO USA Webb Waring Inst Biomed Res Denver CO USA nst Biomed Res, Denver, CO USA Nagoya City Univ, Sch Med, Dept Internal Med 1, Nagoya, Aichi 467, Japan Nagoya City Univ Nagoya Aichi Japan 467 l Med 1, Nagoya, Aichi 467, Japan Louisiana State Univ, Hlth Sci Ctr, Dept Mol & Cellular Physiol, Shreveport, LA 71130 USA Louisiana State Univ Shreveport LA USA 71130 ol, Shreveport, LA 71130 USA
Titolo Testata:
AIDS
fascicolo: 5, volume: 14, anno: 2000,
pagine: 475 - 482
SICI:
0269-9370(20000331)14:5<475:HTIESP>2.0.ZU;2-J
Fonte:
ISI
Lingua:
ENG
Soggetto:
HUMAN-IMMUNODEFICIENCY-VIRUS; JUNCTIONAL PROTEINS; FLK-1/KDR RECEPTOR; FOCAL ADHESION; AIDS PATIENTS; GENE-PRODUCT; CELLS; EXPRESSION; INFECTION; INVITRO;
Keywords:
HIV-1; Tat; vascular permeability; signal transduction;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
36
Recensione:
Indirizzi per estratti:
Indirizzo: Alexander, JS Louisiana State Univ, Med Ctr, Dept Mol & Cellular Physiol, 1501 Kings Highway, Shreveport, LA 71130 USA Louisiana State Univ 1501 Kings Highway Shreveport LA USA 71130
Citazione:
T. Oshima et al., "HIV-1 Tat increases endothelial solute permeability through tyrosine kinase and mitogen-activated protein kinase-dependent pathways", AIDS, 14(5), 2000, pp. 475-482

Abstract

Objective: HIV-1 infection is associated with alterations of several vascular endothelial functions including adhesion molecule expression, growth, and vascular permeability. The bases of these errors are not known, but might involve secretion of the HIV-1 derived transcription factor 'Tat-1'. Thisstudy investigated Tat-1 mediated endothelial barrier changes and second message regulation of this phenomenon. Methods: We exposed human umbilical vein endothelial cell monolayers to Tat-1 (O-150 ng/ml) for up to 48 h and measured resulting changes in monolayer permeability. We also investigated the role of tyrosine and mitogen activated protein (MAP) kinases, and protein kinase C using the pharmacological blockers genistein, PD98059 and KT5823 respectively. Results: Tat-1 significantly reduced monolayer barrier and increased albumin permeability within 23 h. Tat-1 also stimulated tyrosine phosphorylationof multiple endothelial proteins, disorganized junctional phosphotyrosine staining and increased the number of these immunostaining structures. The increased permeability produced by Tat-1 was blocked by genistein and PD98059, but not by KT5823. Genistein and PD98059 pretreatment also prevented thechanges in phosphotyrosine immunostaining produced by Tat-1 and blocked phosphorylation of several proteins including MAP kinase. Conclusion: These results suggest that HIV may dysregulate endothelial barrier through the effects of Tat-1. These blocker experiments suggest that the effects of Tat are transcription/translation-dependent. These data demonstrate that Tat increases endothelial albumin permeability in vitro throughtyrosine kinase and MAP kinase, but not protein kinase G pathways. (C) 2000 Lippincott Williams & Wilkins.

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Documento generato il 02/04/20 alle ore 09:15:34