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Titolo:
Role of monocyte chemoattractant protein-1 in cardiovascular remodeling induced by chronic blockade of nitric oxide synthesis
Autore:
Koyanagi, M; Egashira, K; Kitamoto, S; Ni, WH; Shimokawa, H; Takeya, M; Yoshimura, T; 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 Kumamoto Univ, Sch Med, Dept Pathol 2, Kumamoto 860, Japan Kumamoto Univ Kumamoto Japan 860 Med, Dept Pathol 2, Kumamoto 860, Japan NCI, Immunobiol Lab, Immunopathol Sect, Frederick, MD 21701 USA NCI Frederick MD USA 21701 ab, Immunopathol Sect, Frederick, MD 21701 USA
Titolo Testata:
CIRCULATION
fascicolo: 18, volume: 102, anno: 2000,
pagine: 2243 - 2248
SICI:
0009-7322(20001031)102:18<2243:ROMCPI>2.0.ZU;2-M
Fonte:
ISI
Lingua:
ENG
Soggetto:
LONG-TERM BLOCKADE; CONVERTING ENZYME-ACTIVITY; ANGIOTENSIN-II; ENDOTHELIAL-CELLS; ATHEROSCLEROTIC LESIONS; CHEMOTACTIC PROTEIN-1; MONOCLONAL-ANTIBODY; EXPRESSION; RATS; INHIBITION;
Keywords:
endothelium-derived factors; remodeling; growth substances; inflammation; cell adhesion molecules; proteins;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
34
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:
M. Koyanagi et al., "Role of monocyte chemoattractant protein-1 in cardiovascular remodeling induced by chronic blockade of nitric oxide synthesis", CIRCULATION, 102(18), 2000, pp. 2243-2248

Abstract

Background-Chronic inhibition of endothelial nitric oxide (NO) synthesis by the administration of N-omega-nitro-L-arginine methyl ester (L-NAME) to rats induces early vascular inflammatory changes (monocyte infiltration intocoronary vessels and monocyte chemoattractant protein-1 [MCP-1] expression) as well as subsequent arteriosclerosis (medial thickening and perivascular fibrosis) and cardiac fibrosis. However, the role of MCP-1 in this process is not known. Methods and Results-We investigated the effect of a specific monoclonal anti-MCP-1 neutralizing antibody in rats treated with L-NAME to determine therole of monocytes in the regulation of cardiovascular remodeling. We foundincreased expression of MCP-1 mRNA in vascular endothelial cells and monocytes in inflammatory lesions, Cotreatment with an anti-MCP-1 antibody, but not with control IgG, prevented the L-NAME-induced early inflammation and reduced late coronary vascular medial thickening. In contrast, the anti-MCP-1 antibody did not decrease the development of perivascular fibrosis, the expression of transforming growth factor (TGF)-beta (1) mRNA, or systolic pressure overload induced by L-NAME administration. Conclusions-These results suggest that MCP-1 is necessary for the development of medial thickening as well as monocyte recruitment, In contrast, the pathogenesis of fibrosis may involve other factors, such as TGF-beta (1).

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 31/03/20 alle ore 16:29:43