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Titolo:
Role of transforming growth factor-beta 1 in cardiovascular inflammatory changes induced by chronic inhibition of nitric oxide synthesis
Autore:
Koyanagi, M; Egashira, K; Kubo-Inoue, M; Usui, M; Kitamoto, S; Tomita, H; Shimokawa, H; 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
Titolo Testata:
HYPERTENSION
fascicolo: 1, volume: 35, anno: 2000,
parte:, 1
pagine: 86 - 90
SICI:
0194-911X(200001)35:1<86:ROTGF1>2.0.ZU;2-0
Fonte:
ISI
Lingua:
ENG
Soggetto:
LONG-TERM BLOCKADE; ENDOTHELIUM-DEPENDENT VASODILATION; ANGIOTENSIN-II; FACTOR-BETA; CARDIAC FIBROSIS; CORONARY-ARTERY; RISK-FACTORS; RATS; ACETYLCHOLINE; RECEPTORS;
Keywords:
endothelium-derived factor; growth substances; inflammation; adhesion molecule; angiotensin II; fibrosis;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
29
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 transforming growth factor-beta 1 in cardiovascular inflammatory changes induced by chronic inhibition of nitric oxide synthesis", HYPERTENSIO, 35(1), 2000, pp. 86-90

Abstract

We previously reported that chronic inhibition of nitric oxide (NO) synthesis with N-omega-nitro-L-arginine methyl ester (L-NAME) induces inflammatory changes (monocyte infiltration, myofibroblast formation, and monocyte chemoattractant protein-1 [MCP-1] and transforming growth factor-beta 1 [TGF-beta 1] expression) in the rat heart and vessel. There is debate regarding whether TGF-beta 1 exhibits proinflammatory or anti-inflammatory activities. We used the rat model to investigate the role of TGF-beta in the pathogenesis of such inflammatory changes. We show here that infiltrating monocytes and myofibroblasts in the inflammatory lesions produced TGF-beta 1 on the third day of L-NAME administration. Cotreatment with a monoclonal antibody against TGF-beta 1, but not with control IgG, prevented the L-NAME-induced cardiac inflammation. The antibody also significantly inhibited the gene expression of MCP-1, P-selectin, and intercellular adhesion molecule-1. In summary, the antibody against TGF-beta 1 prevented inflammatory changes in ratheart and vessel induced by chronic inhibition of NO synthesis, suggestingthat increased production of TGF-beta 1 is involved in the: inflammatory changes in this model.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/04/20 alle ore 08:07:34