Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Adenovirus-mediated overexpression of dominant-negative mutant of c-Jun prevents intercellular adhesion molecule-1 induction by LDL - A critical rolefor activator protein-1 in endothelial activation
Autore:
Wang, NP; Verna, L; Liao, HL; Ballard, A; Zhu, Y; Stemerman, MB;
Indirizzi:
Univ Calif Riverside, Div Biomed Sci, Riverside, CA 92521 USA Univ Calif Riverside Riverside CA USA 92521 Sci, Riverside, CA 92521 USA
Titolo Testata:
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
fascicolo: 9, volume: 21, anno: 2001,
pagine: 1414 - 1420
SICI:
1079-5642(200109)21:9<1414:AOODMO>2.0.ZU;2-T
Fonte:
ISI
Lingua:
ENG
Soggetto:
LOW-DENSITY-LIPOPROTEIN; NF-KAPPA-B; TRANSCRIPTION FACTORS AP-1; NITRIC-OXIDE SYNTHASE; GENE-EXPRESSION; CELLS; STRESS; CONSTRUCTION; MECHANISM; VECTORS;
Keywords:
LDL; endothelium; adhesion molecules; transcription factors; gene expression;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
39
Recensione:
Indirizzi per estratti:
Indirizzo: Wang, NP Univ Calif Riverside, Div Biomed Sci, Riverside, CA 92521 USA Univ Calif Riverside Riverside CA USA 92521 erside, CA 92521 USA
Citazione:
N.P. Wang et al., "Adenovirus-mediated overexpression of dominant-negative mutant of c-Jun prevents intercellular adhesion molecule-1 induction by LDL - A critical rolefor activator protein-1 in endothelial activation", ART THROM V, 21(9), 2001, pp. 1414-1420

Abstract

Low density lipoprotein (LDL) induces intercellular adhesion molecule-1 (ICAM-1) gene expression and leads to endothelial cell (EC) leukocyte adhesion. However, the transcriptional mechanism for LDL-induced EC perturbation remains to be fully explained. Activator protein-1 (AP-1) is induced after the exposure of ECs to LDL. In the present study, a regulated adenovirus expressing a dominant-negative mutant of c-Jun (TAM-67) was used to examine the role of AP-1 in the LDL-induced ICAM-1 activation. Overexpression of TAM-67 specifically inhibited AP-1 activation and prevented the LDL-activated surface expression of ICAM-1 protein in human umbilical vein ECs and human coronary artery ECs. Northern analyses and promoter transactivation assays indicated that this effect of TAM-67 was likely mediated through a suppression of the transcriptional regulation of the ICAM-1 gene. Functionally, TAM-67 attenuated leukocyte adherence to ECs in response to LDL. Furthermore, electrophoresis mobility shift assays and site-directed mutagenesis suggested that an AP-1-like motif in the promoter region of the human ICAM-1 gene was a critical cis element for LDL induction. These results, for the first time, provide evidence suggesting that AP-1 is a major regulatory mechanism leading to endothelial activation.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/04/20 alle ore 10:49:25