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This Article Full Text Full Text (PDF) All Versions of this Article: 289/1/E105    most recent 00366.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Rzewuska-Lech, E. Articles by Miller, V. M. Search for Related Content PubMed PubMed Citation Articles by Rzewuska-Lech, E. Articles by Miller, V. M.

Differential effects of 17-estradiol and raloxifene on VSMC phenotype and expression of osteoblast-associated proteins

Departments of ¹Surgery, ²Internal Medicine, Division of Endocrinology, and ³Physiology and Bioengineering, Mayo Clinic College of Medicine, Rochester, Minnesota

Submitted 12 August 2004 ; accepted in final form 7 February 2005

Several studies demonstrate an association between osteoporosis and arterial calcific disease, both of which being common in elderly women. Estradiol and raloxifene, a selective estrogen receptor modulator, prevent bone loss in postmenopausal women. Little is known regarding how these agents affect arterial calcification. The aim of this study was to determine whether or not 17-estradiol and raloxifene reduced vascular smooth muscle cell (VSMC) differentiation and expression of bone-associated proteins during phosphate-induced calcification in vitro. Aortic VSMC were cultured from adult, gonadally intact, and ovariectomized (OVX) female pigs. Calcifying medium was added, and cells were treated with solvent (control), 17-estradiol (E₂), or raloxifene. Extent of calcification and phenotypic expression of bone-associated proteins [matrix gla protein (MGP), osteoprotegerin (OPG), and bone sialoprotein (BSP)] were examined at 3-day intervals over 2 wk. Calcium content increased in all groups but was greater in VSMC derived from intact compared with OVX animals. E₂ reduced calcification and preserved a contractile phenotype. Expression of OPG significantly decreased with time; this decrease was significantly greater in VSMC derived from OVX compared with gonadally intact pigs. E₂ and raloxifene preserved expression of OPG only in VSMC from intact pigs. Expression of MGP increased significantly with time and was not affected by E₂ or raloxifene treatments. E₂ treatment significantly inhibited synthesis of BSP in cells from both groups. In conclusion, E₂ slows differentiation of VSMC induced by excess phosphate. Effectiveness of raloxifene to preserve expression of bone cell-associated proteins depends on the hormonal status of the tissue donor.

vascular smooth muscle cells; estrogen; raloxifene; selective receptor modulator; smooth muscle phenotype

This article has been cited by other articles:

				V. M. Miller and S. P. Duckles Vascular Actions of Estrogens: Functional Implications Pharmacol. Rev., June 1, 2008; 60(2): 210 - 241. [Abstract] [Full Text] [PDF]