Pour savoir comment effectuer et gérer un dépôt de document, consultez le « Guide abrégé – Dépôt de documents » sur le site Web de la Bibliothèque. Pour toute question, écrivez à corpus@ulaval.ca.
 

Personne :
Carter, Sophie

En cours de chargement...
Photo de profil

Adresse électronique

Date de naissance

Projets de recherche

Structures organisationnelles

Fonction

Nom de famille

Carter

Prénom

Sophie

Affiliation

Université Laval.Faculté de pharmacie

ISNI

ORCID

Identifiant Canadiana

ncf13720924

person.page.name

Résultats de recherche

Voici les éléments 1 - 2 sur 2
  • PublicationRestreint
    Relationship between insulin-like growth factor binding protein-2 and left ventricular stroke volume in patients with aortic stenosis.
    (Canadian Cardiology Publications., 2015-12-01) Carter, Sophie; Picard, Frédéric; Bédard, Élisabeth; Capoulade, Romain; Pibarot, Philippe; Dumesnil, Jean G.; Mathieu, Patrick; Arsenault, Marie
    Background : Lower plasma insulin-like growth factor binding protein (IGFBP)-2 levels have been associated with altered metabolism linked to visceral obesity. These abnormalities have been linked with worsening of left ventricle (LV) remodelling and dysfunction in patients with aortic stenosis (AS). Whether IGFBP-2 is involved in these relationships is currently unknown. The objective of this study was to examine the relationship between circulating IGFBP-2 and LV pump function measured according to stroke volume index in AS patients with preserved LV ejection fraction. Methods : Two hundred eight patients with mild to moderate AS were prospectively recruited in the Metabolic Determinants of the Progression of Aortic Stenosis (PROGRESSA) study and underwent Doppler-echocardiography. Stroke volume index (SVi) was calculated using Doppler in the LV outflow tract and was indexed to body surface area. Plasma circulating IGFBP-2 levels were measured using an enzyme-linked immunosorbent assay. Results : Patients with lower IGFBP-2 levels were younger (P < 0.0001), had a higher body mass index (P = 0.0003), larger waist circumference (P = 0.01), higher homeostatic assessment model index (P = 0.0005), and lower high-density lipoprotein cholesterol (P = 0.01). Moreover, SVi was decreased in patients with low IGFBP-2 (P = 0.009). After multivariable adjustment for age, sex, LV mass index, aortic valve area, and LV ejection fraction, a lower plasma IGFBP-2 level was independently related with lower SVi (P < 0.001). After further adjustment for other traditional cardiometabolic risk factors, plasma IGFBP-2 remained independently associated with SVi (all P < 0.05). Conclusions : In this study, we documented that lower IGFBP-2 levels are independently associated with lower SVi, a powerful predictor of worse outcomes in the mild to moderate AS population.
  • PublicationAccès libre
    Sirt1 inhibits resistin expression in aortic stenosis
    (Public Library of Science, 2012-04-06) Carter, Sophie; Roy-Bellavance, Catherine; Picard, Frédéric; Boivin, Louise; Li, Zhuo; Pibarot, Philippe; Mathieu, Patrick; Miard, Stéphanie
    The development of human calcified aortic stenosis (AS) includes age-dependent processes that have been involved in atherosclerosis, such as infiltration of macrophages in aortic valves, which then promote production of many pro-inflammatory cytokines, including resistin. However, the molecular mechanisms contributing to these processes are not established. Since Sirt1 has been shown to modulate macrophage biology and inflammation, we examined its levels in human AS and tested its impact on resistin expression. Sirt1 mRNA (p = 0.01) and protein (p<0.05) levels were reduced in explanted valves from AS patients (n = 51) compared to those from control (n = 11) patients. Sirt1 mRNA levels were negatively associated with resistin mRNA levels quantified in AS valves (p = 0.02). Stimulation of Sirt1 by resveratrol or virus-driven overexpression robustly diminished resistin mRNA and protein expression in macrophages, whereas down-regulation of Sirt1 triggered a large increase in resistin expression. These effects were direct, as chromatin immunoprecipitation assays showed that Sirt1 physically interacted with the resistin promoter region at an AP-1 response element. Moreover, Sirt1 blocked c-jun-induced resistin transactivation in gene reporter assays. These findings demonstrate that, in calcified AS, levels of Sirt1 are reduced whereas those of resistin are increased within aortic valve leaflets. Our results also suggest that this loss of Sirt1 expression alleviates its inhibition of resistin transcription in macrophages. Although the overall contribution of this process to the underlying mechanisms for AS disease development remains unresolved, these observations suggest that modification of Sirt1 expression and/or activity could represent a novel approach against inflammation in AS.