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Titolo:
Phosphate regulation of vascular smooth muscle cell calcification
Autore:
Jono, S; McKee, MD; Murry, CE; Shioi, A; Nishizawa, Y; Mori, K; Morii, H; Giachelli, CM;
Indirizzi:
Univ Washington, Dept Bioengn, Seattle, WA 98195 USA Univ Washington Seattle WA USA 98195 Dept Bioengn, Seattle, WA 98195 USA Univ Washington, Dept Pathol, Seattle, WA 98195 USA Univ Washington Seattle WA USA 98195 , Dept Pathol, Seattle, WA 98195 USA McGill Univ, Dept Dent, Montreal, PQ, Canada McGill Univ Montreal PQ Canada ill Univ, Dept Dent, Montreal, PQ, Canada McGill Univ, Dept Cell Biol & Anat, Montreal, PQ, Canada McGill Univ Montreal PQ Canada pt Cell Biol & Anat, Montreal, PQ, Canada Osaka City Univ, Sch Med, Dept Internal Med 2, Osaka 545, Japan Osaka CityUniv Osaka Japan 545 d, Dept Internal Med 2, Osaka 545, Japan
Titolo Testata:
CIRCULATION RESEARCH
fascicolo: 7, volume: 87, anno: 2000,
pagine: E10 - E17
SICI:
0009-7330(20000929)87:7<E10:PROVSM>2.0.ZU;2-J
Fonte:
ISI
Lingua:
ENG
Soggetto:
TRANSPORTER RETROVIRUS RECEPTOR; NA/P-I-COTRANSPORTER; OSTEOBLAST DIFFERENTIATION; CORONARY-ARTERIES; MATRIX VESICLES; AORTIC-VALVE; OSTEOPONTIN; EXPRESSION; CLONING; GENE;
Keywords:
vascular calcification; hyperphosphatemia; inorganic phosphate; human smooth muscle cell; sodium-dependent phosphate transport; Pit-1; Cbfa-1;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
48
Recensione:
Indirizzi per estratti:
Indirizzo: Giachelli, CM Univ Washington, Dept Bioengn, Box 351720,Bagley Hall,Room 479, Seattle, WA 98195 USA Univ Washington Box 351720,Bagley Hall,Room 479 Seattle WA USA 98195
Citazione:
S. Jono et al., "Phosphate regulation of vascular smooth muscle cell calcification", CIRCUL RES, 87(7), 2000, pp. E10-E17

Abstract

Vascular calcification is a common finding in atherosclerosis and a serious problem in diabetic and uremic patients. Because of the correlation of hyperphosphatemia and vascular calcification, the ability of extracellular inorganic phosphate levels to regulate human aortic smooth muscle cell (HSMC)culture mineralization in vitro was examined. HSMCs cultured in media containing normal physiological levels of inorganic phosphate (1.4 mmol/L) did not mineralize. In contrast, HSMCs cultured in media containing phosphate levels comparable to those seen in hyperphosphatemic individuals (>1.4 mmol/L) showed dose-dependent increases in mineral deposition. Mechanistic studies revealed that elevated phosphate treatment of HSMCs also enhanced the expression of the osteoblastic differentiation markers osteocalcin and Osf2/Cbfa-1. The effects of elevated phosphate on HSMCs were mediated by a sodium-dependent phosphate cotransporter (NPC), as indicated by the ability of the specific NPC inhibitor phosphonoformic acid, to dose dependently inhibit phosphate-induced calcium deposition as well as osteocalcin and Cbfa-1 geneexpression, With the use of polymerase chain reaction and Northern blot analyses, the NPC in HSMCs was identified as Pit-1 (Glvr-1), a member of the novel type III NPCs, These data suggest that elevated phosphate may directly stimulate HSMCs to undergo phenotypic changes that predispose to calcification and offer a novel explanation of the phenomenon of vascular calcification under hyperphosphatemic conditions. The full text of this article is available at http://www.circresaha.org.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 20/09/20 alle ore 10:42:50