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Selective estrogen receptor modulators prevent neointima formation after vascular injury.

Abstract：

:Exploitation of estrogen's vasculoprotective properties in drug design is difficult due to its adverse effects on endometrium and breast. Selective estrogen receptor modulators (SERM) act as estrogen agonists in some tissues but are anti-estrogenic in others. We investigate here whether tamoxifen, raloxifene, and two novel SERMs, ospemifene and fispemifene, preserve estrogen's beneficial effects on the ovariectomized rat vascular wall, and correlate their effects with natural estrogen (17beta-E2) and a pure anti-estrogen ICI 182,780. All compounds dose-dependently (0.0025-25 mg/kg/day) inhibited neointimal thickening at 7 days after aorta denudation injury. At 28 days, tamoxifen and ospemifene (2.5 mg/kg/day) reduced intimal nuclei number and intimal area equal to 17beta-E2, while raloxifene and fispemifene had no effect. Replacing the drug at 14 days with vehicle did not induce any rebound effect at 28 days, and furthermore, resulted in a smaller neointima with raloxifene and fispemifene. 17beta-E2 and the SERMs also significantly enhanced reendothelialization. All compounds inhibited replication and all but fispemifene inhibited migration of vascular SMC and cells from cultured aortic explants in vitro. Finally, only 17beta-E2 increased the weight of the uterus above that of normal rats. Interestingly, ICI 182,780 also weakly inhibited neointima formation and SMC proliferation at 7 days, suggesting that non-estrogen receptor mediated effects may have also played a role. In conclusion, SERMs have beneficial estrogen agonist effects in the injured vascular wall through their regulation of vascular SMC function and reendothelialization. Early intervention is of particular importance in preventing the injury-response.

journal_name

Mol Cell Endocrinol

journal_title

Molecular and cellular endocrinology

authors

Savolainen-Peltonen H,Luoto NM,Kangas L,Häyry P

doi

10.1016/j.mce.2004.08.004

keywords:

subject

Has Abstract

pub_date

2004-11-30 00:00:00

pages

9-20

issue

1-2

eissn

0303-7207

issn

1872-8057

pii

S0303-7207(04)00310-7

journal_volume

227

pub_type

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