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Titolo:
Diltiazem, a calcium antagonist, inhibits matrix metalloproteinase-1 (tissue collagenase) production and collagenolytic activity in human vascular smooth muscle cells
Autore:
Wada, Y; Kato, S; Okamoto, K; Izumaru, S; Aoyagi, S; Morimatsu, M;
Indirizzi:
Kurume Univ, Sch Med, Dept Pathol, Kurume, Fukuoka 8300011, Japan Kurume Univ Kurume Fukuoka Japan 8300011 , Kurume, Fukuoka 8300011, Japan Kurume Univ, Sch Med, Dept Surg, Kurume, Fukuoka 8300011, Japan Kurume Univ Kurume Fukuoka Japan 8300011 , Kurume, Fukuoka 8300011, Japan
Titolo Testata:
INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE
fascicolo: 5, volume: 8, anno: 2001,
pagine: 561 - 566
SICI:
1107-3756(200111)8:5<561:DACAIM>2.0.ZU;2-E
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROTEIN-KINASE-C; GROWTH-FACTOR; CHANNEL BLOCKERS; ENDOTHELIAL-CELLS; MESSENGER-RNA; PROLIFERATION; EXPRESSION; CA2+; APOPTOSIS; INVOLVEMENT;
Keywords:
smooth muscle cell; calcium antagonist; matrix metalloproteinase; vascular remodeling;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
44
Recensione:
Indirizzi per estratti:
Indirizzo: Kato, S Kurume Univ, Sch Med, Dept Pathol, 67 Asahi Machi, Kurume, Fukuoka8300011, Japan Kurume Univ 67 Asahi Machi Kurume Fukuoka Japan 8300011 011, Japan
Citazione:
Y. Wada et al., "Diltiazem, a calcium antagonist, inhibits matrix metalloproteinase-1 (tissue collagenase) production and collagenolytic activity in human vascular smooth muscle cells", INT J MOL M, 8(5), 2001, pp. 561-566

Abstract

Calcium antagonists (CAs) are widely prescribed for patients with cardiovascular diseases. CAs have been reported to inhibit smooth muscle cell (SMC)proliferation in addition to their effects on vascular tone. To determine whether CAs potentially affect vascular remodeling, we measured the expression of matrix-degrading, enzymes in growth factor-stimulated SMC. Human cultured SMC were stimulated with 10 ng/ml of platelet-derived growth factor (PDGF)-BB with or without a calcium antagonist, diltiazem. In the cell counting assay, diltiazem (10(-5) M) alone had no effect on the proliferation ofquiescent SMC, however 10(-6)-10(-5) M of diltiazem dose-dependently inhibited PDGF-stimulated SMC proliferation. The inhibitory effects of diltiazemon SMC proliferation were further confirmed by a 5-bromo-2'-deoxyuridine (BrdU) incorporation assay and flow cytometry. In Western blotting, matrix metalloproteinase (MMP)-1 (tissue collagenase) but not MMP-2 (72-kDa gelatinase) expression was upregulated by PDGF and phorbol ester (TPA), which werereduced by diltiazem in a dose-dependent manner. The downregulation of MMP-1 expression was consistent with the reduction of collagenolytic activity measured by a FITC-conjugated type I collagen breakdown assay. PDGF-stimulated c-Jun/AP-1 expression, a major transcriptional factor for MMP-1, was not affected by diltiazem. In contrast, intracellular calcium ions measured with a fluorometric assay of Fluo-3AM-loaded cells revealed that the PDGF-stimulated increase in the intracellular calcium content was dose-dependentlyreduced by diltiazem. Our data suggest that diltiazem inhibits not only proliferation but also MMP-1 expression and collagenolytic activity in PDGF-stimulated SMC. The administration of CAs potentially influences the processof vascular remodeling, and this possibility should be further verified invivo.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 12/07/20 alle ore 06:52:16