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Titolo:
Anti-monocyte chemoattractant protein-1 gene therapy inhibits vascular remodeling in rats: blockade of MCP-1 activity after intramuscular transfer ofa mutant gene inhibits vascular remodeling induced by chronic blockade of NO synthesis
Autore:
Egashira, K; Koyanagi, M; Kitamoto, S; Ni, WH; Kataoka, C; Morishita, R; Kaneda, Y; Akiyama, C; Nishida, KI; Sueishi, K; Takeshita, A;
Indirizzi:
Kyushu Univ, Grad Sch Med Sci, Dept Cardiovasc Med, Higashi Ku, Fukuoka 8128582, Japan Kyushu Univ Fukuoka Japan 8128582 ed, Higashi Ku, Fukuoka 8128582, Japan Kyushu Univ, Grad Sch Med Sci, Dept Pathol, Higashi Ku, Fukuoka 8128582, Japan Kyushu Univ Fukuoka Japan 8128582 ol, Higashi Ku, Fukuoka 8128582, Japan Osaka Univ, Sch Med, Div Gene Therapy Sci, Osaka, Japan Osaka Univ OsakaJapan niv, Sch Med, Div Gene Therapy Sci, Osaka, Japan Daiichi Pharmaceut Co Ltd, New Prod Res Labs, Tokyo, Japan Daiichi Pharmaceut Co Ltd Tokyo Japan , New Prod Res Labs, Tokyo, Japan
Titolo Testata:
FASEB JOURNAL
fascicolo: 13, volume: 14, anno: 2000,
pagine: 1974 - 1978
SICI:
0892-6638(200010)14:13<1974:ACPGTI>2.0.ZU;2-K
Fonte:
ISI
Lingua:
ENG
Soggetto:
NITRIC-OXIDE SYNTHESIS; ATHEROSCLEROTIC LESIONS; EXPRESSION; CHEMOKINES; INDUCTION; MICE;
Keywords:
endothelium-derived relaxing factors; remodeling; growth substances; inflammation; adhesion molecule; monocyte chemoattractant protein-1; gene transfer;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
19
Recensione:
Indirizzi per estratti:
Indirizzo: Egashira, K Kyushu Univ, Grad Sch Med Sci, Dept Cardiovasc Med, Higashi Ku, 3-1-1 Maidashi, Fukuoka 8128582, Japan Kyushu Univ 3-1-1 Maidashi Fukuoka Japan 8128582 28582, Japan
Citazione:
K. Egashira et al., "Anti-monocyte chemoattractant protein-1 gene therapy inhibits vascular remodeling in rats: blockade of MCP-1 activity after intramuscular transfer ofa mutant gene inhibits vascular remodeling induced by chronic blockade of NO synthesis", FASEB J, 14(13), 2000, pp. 1974-1978

Abstract

Monocyte chemoattractant protein-1 (MCP-1) may play an essential part in the formation of arteriosclerosis by recruiting monocytes into the arterial wall. Thus, we devised a new strategy for anti-MCP-1 gene therapy against arteriosclerosis by transfecting an amino-terminal deletion mutant (missing the amino-terminal amino acids 2 to 8) of the human MCP-1 gene into a remote organ (skeletal muscles), Intramuscular transduction with the mutant MCP-1 gene blocked monocyte recruitment induced by a subcutaneous injection of recombinant MCP-1. In a rat model in which the chronic inhibition of endothelial nitric oxide synthesis induces early vascular inflammation as well assubsequent coronary vascular remodeling, this strategy suppressed monocyterecruitment into the coronary vessels and the development of vascular medial thickening, but did not reduce perivascular fibrosis. Thus, MCP-1 is necessary far the development of medial thickening but not for fibrosis in this model. This new strategy may be a useful and feasible gene therapy against arteriosclerosis.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 09/04/20 alle ore 12:45:29