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Bouchareb, Rihab

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Bouchareb

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Rihab

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Université Laval

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Voici les éléments 1 - 3 sur 3
  • PublicationAccès libre
    Soluble CD14 is associated with the structural failure of bioprostheses
    (Elsevier, 2018-06-30) Dahou, Abdellaziz; Bouchareb, Rihab; Arsenault, Benoit; Mkannez, Ghada; Boulanger, Marie-Chloé; Bossé, Yohan; Pibarot, Philippe; Clavel, Marie-Annick; Nsaibia, Mohamed Jalloul; Mathieu, Patrick; Salaun, Erwan
    Introduction: Aortic valve bioprostheses, which do not mandate chronic anticoagulation, are prone to structural valve degeneration (SVD). The processes involved in SVD are likely multifactorial. We hypothesized that inflammation and macrophage activation could be involved in SVD. Methods: In 203 patients with an aortic valve bioprosthesis, we evaluated the association between the macrophage activation marker soluble CD14 (sCD14) and SVD. Results: After a mean follow-up of 8 ± 3 years, 42 (21%) patients developed SVD. Patients with SVD had higher peak (44 ± 13 mmHg vs. 25 ± 12 mmHg, p < .0001) and mean (24 ± 7 mmHg vs. 12 ± 5 mmHg, p < .0001) transprosthetic gradients. On univariable analysis, low-density lipoprotein cholesterol (LDL) and sCD14 were associated with SVD. After correction for covariates, sCD14 (OR: 1.12, 95%CI: 1.02–1.23, p = .01) remained independently associated with SVD. In turn, sCD14 was associated with the HOMA index and high-density lipoprotein (HDL) level. Patients with a metabolic syndrome (MetS) had higher level of sCD14. In a model corrected for age, sex, HOMA and HDL, the MetS remained independently associated with sCD14 levels (β = 0.65, SE = 0.30, p = .03). Conclusion: Circulating level of sCD14 is an independent predictor of SVD. In turn, patients with MetS have higher sCD14 levels.
  • PublicationRestreint
    Autotaxin interacts with lipoprotein(a) and oxidized phospholipids in predicting the risk of calcific aortic valve stenosis in patients with coronary artery disease
    (Blackwell Scientific Publication, 2020-05-30) Simard, Sébastien; Bouchareb, Rihab; Arsenault, Benoit; Boulanger, Marie-Chloé; Bossé, Yohan; Mahmut, Ablajan; Witztum, Joseph L.; Pibarot, Philippe; Clavel, Marie-Annick; Nsaibia, Mohamed Jalloul; Mathieu, Patrick; Tsimikas, Sotirios
    Background Studies have shown that lipoprotein(a) [Lp(a)], an important carrier of oxidized phospholipids, is causally related to calcific aortic valve stenosis (CAVS). Recently, we found that Lp(a) mediates the development of CAVS through autotaxin (ATX). Objective To determine the predictive value of circulating ATX mass and activity for CAVS. Methods We performed a case-control study in 300 patients with coronary artery disease (CAD). Patients with CAVS plus CAD (cases, n = 150) were age- and gender-matched (1 : 1) to patients with CAD without aortic valve disease (controls, n = 150). ATX mass and enzymatic activity and levels of Lp(a) and oxidized phospholipids on apolipoprotein B-100 (OxPL-apoB) were determined in fasting plasma samples. Results Compared to patients with CAD alone, ATX mass (P < 0.0001), ATX activity (P = 0.05), Lp(a) (P = 0.003) and OxPL-apoB (P < 0.0001) levels were elevated in those with CAVS. After adjustment, we found that ATX mass (OR 1.06, 95% CI 1.03–1.10 per 10 ng mL−1, P = 0.001) and ATX activity (OR 1.57, 95% CI 1.14–2.17 per 10 RFU min−1, P = 0.005) were independently associated with CAVS. ATX activity interacted with Lp(a) (P = 0.004) and OxPL-apoB (P = 0.001) on CAVS risk. After adjustment, compared to patients with low ATX activity (dichotomized at the median value) and low Lp(a) (<50 mg dL−1) or OxPL-apoB (<2.02 nmol L−1, median) levels (referent), patients with both higher ATX activity (≥84 RFU min−1) and Lp(a) (≥50 mg dL−1) (OR 3.46, 95% CI 1.40–8.58, P = 0.007) or OxPL-apoB (≥2.02 nmol L−1, median) (OR 5.48, 95% CI 2.45–12.27, P < 0.0001) had an elevated risk of CAVS. Conclusion Autotaxin is a novel and independent predictor of CAVS in patients with CAD.
  • PublicationRestreint
    Altered DNA methylation of long noncoding RNA H19 in calcific aortic valve disease promotes mineralization by silencing NOTCH1
    (American Heart Association, 2016-12-06) Gaudreault, Nathalie; Bouchareb, Rihab; Guay, Simon-Pierre; Amellah, Soumiya; Mkannez, Guada; Tremblay-Marchand, Joël; Boulanger, Marie-Chloé; Guauque-Olarte, Sandra; Bossé, Yohan; Pibarot, Philippe; Hadji, Fayez; Bouchard, Luigi; Nsaibia, Mohamed Jalloul; Mathieu, Patrick
    Background: Calcific aortic valve disease is characterized by an abnormal mineralization of the aortic valve. Osteogenic activity in the aortic valve is under the control of NOTCH1, which regulates the expression of key pro-osteogenic genes such as RUNX2 and BMP2. Long noncoding RNAs (lncRNAs) may reprogram cells by altering the gene expression pattern. Methods: Multidimensional genomic profiling was performed in human aortic valves to document the expression of lncRNAs and the DNA methylation pattern in calcific aortic valve disease. In-depth functional assays were carried out to document the impact of lncRNA on the mineralization of the aortic valve. Results: We documented that lncRNA H19 (H19) was increased in calcific aortic valve disease. Hypomethylation of the promoter region was observed in mineralized aortic valves and was inversely associated with H19 expression. Knockdown and overexpression experiments showed that H19 induces a strong osteogenic phenotype by altering the NOTCH1 pathway. Gene promoter analyses showed that H19 silenced NOTCH1 by preventing the recruitment of p53 to its promoter. A knockdown of H19 in valve interstitial cells (VICs) increased the expression of NOTCH1 and decreased the level of RUNX2 and BMP2, 2 downstream targets repressed by NOTCH1. In rescue experiments, the transfection of a vector encoding for the active Notch intracellular domain prevented H19-induced mineralization of valve interstitial cells. Conclusions: These findings indicate that a dysregulation of DNA methylation in the promoter of H19 during calcific aortic valve disease is associated with a higher expression of this lncRNA, which promotes an osteogenic program by interfering with the expression of NOTCH1.