Timing of the vascular actions of estrogens in experimental and human studies: Why protective early, and not when delayed?

Lenfant, Françoise; Trémollières, Florence; Gourdy, Pierre; Arnal, Jean‐François

doi:10.1016/j.maturitas.2010.11.016

Cited by 64 publications

(69 citation statements)

References 105 publications

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“…24 The mechanisms accounting for the impact of timing in the atheroprotective action of estrogens has been recently reviewed. 15 In particular, it has been described, in the atheroma plaque, a decreased ERα expression 16,25 and an increase in 27-hydroxycholesterol (27HC) production. 26 Indeed, 27HC is a competitive antagonist of ER action, which can counteract the protective action of 17-β-estradiol (E2).…”

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confidence: 99%

“…15 The initial results suggested a negative impact of the treatment, leading to a worldwide reduction in the use of substitution therapies. Nevertheless, recent publications with a more detailed analysis of the data countermanded the initial conclusion.…”

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confidence: 99%

“…14 Epidemiological studies have demonstrated that women, before menopause, are better protected than men against cardiovascular diseases. 15 Indeed, vascular and heart cells contain specific high-affinity receptors for estrogen in both humans 16 and animals. 17 Furthermore, estrogens stimulate eNOS leading to NO production.…”

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Determinants of Flow-Mediated Outward Remodeling in Female Rodents

Tarhouni

Guihot

Vessières

et al. 2014

ATVB

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Objective-Flow (shear stress)-mediated outward remodeling (FMR) of resistance arteries is a key adaptive process allowing collateral growth after arterial occlusion but declining with age. 17-β-estradiol (E2) has a key role in this process through activation of estrogen receptor α (ERα). Thus, we investigated the impact of age and timing for estrogen efficacy on FMR. Approach and Results-Female rats, 3 to 18 months old, were submitted to surgery to increase blood flow locally in 1 mesenteric artery in vivo. High-flow and normal-flow arteries were collected 2 weeks later for in vitro analysis. Diameter increased by 27% in high-flow arteries compared with normal-flow arteries in 3-month-old rats. The amplitude of remodeling declined with age (12% in 18-month-old rats) in parallel with E2 blood level and E2 substitution failed restoring remodeling in 18-month-old rats. Ovariectomy of 3-, 9-, and 12-month-old rats abolished FMR, which was restored by immediate E2 replacement. Nevertheless, this effect of E2 was absent 9 months after ovariectomy. In this latter group, ERα and endothelial nitric oxide synthase expression were reduced by half compared with age-matched rats recently ovariectomized. FMR did not occur in ERα −/− mice, whereas it was decreased by 50% in ERα +/− mice, emphasizing the importance of gene dosage in high-flow remodeling. Conclusions-E2 deprivation, rather than age, leads to decline in FMR, which can be prevented by early exogenous E2.However, delayed E2 replacement was ineffective on FMR, underlining the importance of timing of this estrogen action. 15 The initial results suggested a negative impact of the treatment, leading to a worldwide reduction in the use of substitution therapies. Nevertheless, recent publications with a more detailed analysis of the data countermanded the initial conclusion. Interestingly, a major difference in the effect of hormones between younger and older women has been shown. Indeed, the treatment tended to confer coronary protection in women treated within 10 years after menopause, whereas a latter treatment may induce deleterious effects. 24 The mechanisms accounting for the impact of timing in the atheroprotective action of estrogens has been recently reviewed. 15 In particular, it has been described, in the atheroma plaque, a decreased ERα expression 16,25 and an increase in 27-hydroxycholesterol (27HC) production. 26 Indeed, 27HC is a competitive antagonist of ER action, which can counteract the protective action of 17-β-estradiol (E2). 26To better understand to which extent a timing effect also can impact the function of arterioles, we investigated FMR of resistance arteries in young and old female rats and then in young ovariectomized rats as a model of surgical menopause. Materials and MethodsMaterials and Methods are available in the online-only Supplement. Results Estradiol Blood Level and FMRFourteen days after arterial ligation, arterial diameter was determined in vitro in response to stepwise increases in intraluminal pressure. Passive arterial diamet...

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Determinants of Flow-Mediated Outward Remodeling in Female Rodents

Tarhouni

Guihot

Vessières

et al. 2014

ATVB

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“…Le détail de cette structure, révélé par cristallographie aux rayons X, montre que la fixation de sur-risque coronarien n'apparaît que chez les femmes les plus âgées (ce qui est probablement dû à la prise du traitement après 20 ans de ménopause, et donc après une longue période de carence oestrogé-nique). Il semble donc que le mode d'administration du THS soit la clé de l'augmentation du risque de thrombose ; le type de progestatif utilisé apparaît aussi crucial pour le risque de cancer [1,2]. Des modulateurs sélectifs des ER (SERM, selective estrogen receptor modulator) 2 ont été développés dans le cadre du cancer du sein car ils conservent certaines actions bénéfiques (sur l'os par exemple) et s'opposent à certains effets délétères des oestrogènes, en particulier sur la prolifération du cancer du sein ER-positif [3].…”

Section: Le Récepteur Alpha Des Oestrogènes (Era) : Un Récepteur Nuclunclassified

“…Ceci requiert une meilleure compré-hension du mode d'action de leur cible, le récepteur ER . 2 Les SERM sont des molécules capables de se fixer sur les récepteurs des oestrogènes et d'avoir une action à la fois agoniste et antagoniste des oestrogènes. [7].…”

Section: Le Récepteur Alpha Des Oestrogènes (Era) : Un Récepteur Nuclunclassified

Effets membranaires du récepteur alpha des œstrogènes

et al. 2015

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Surface modification of implanted cardiovascular metal stents: From antithrombosis and antirestenosis to endothelialization

Zhang

Liu

et al. 2013

J Biomedical Materials Res

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Driven by the complications occurring with bare metal stents and drug-eluting stents, concerns have been raised over strategies for long-term safety, with respect to preventing or inhibiting stent thrombosis, restenosis, and in-stent restenosis in particularly. Surface modification is very important in constructing a buffer layer at the interface of the organic and inorganic materials and in ultimately obtaining long-term biocompatibility. In this review, we summarize the developments in surface modification of implanted cardiovascular metal stents. This review focuses on the modification of metal stents via coating drugs or biomolecules to enhance antithrombosis, antirestenosis, and/or endothelialization. In addition, we indicate the probable future work involving the modification of the metallic blood-contacting surfaces of stents and other cardiovascular devices that are under development.

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Timing of the vascular actions of estrogens in experimental and human studies: Why protective early, and not when delayed?

Cited by 64 publications

References 105 publications

Determinants of Flow-Mediated Outward Remodeling in Female Rodents

Determinants of Flow-Mediated Outward Remodeling in Female Rodents

Effets membranaires du récepteur alpha des œstrogènes

Surface modification of implanted cardiovascular metal stents: From antithrombosis and antirestenosis to endothelialization

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