Intérêts potentiels des facteurs angiogéniques placentaires comme biomarqueurs dans la pré-éclampsie pour le clinicien

Boulanger, Henri; Lefèvre, Guillaume; Saksi, Salima Ahriz; Achiche, Jedjiga; Bailleul, S.; Ekoukou, Dieudonné; Drouin, Dominique; Sault, Corinne; Stawiarski, Nicolas; DuPuis, E. Melanie

doi:10.1016/j.nephro.2018.10.005

Cited by 5 publications

(2 citation statements)

References 135 publications

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“…Conversely, pro‐angiogenic factors, such as VEGF and PIGF, are markedly decreased in patients with PPCM or PIH/preeclampsia. Mechanistically, sFlt‐1 can compete with VEGF receptors (VEGFR1 and VEGFR2) for VEGF and PIGF binding, preventing the interaction between VEGF/PIGF and VEGFR1/2 19 …”

Section: Discussionmentioning

confidence: 99%

“…Mechanistically, sFlt-1 can compete with VEGF receptors (VEGFR1 and VEGFR2) for VEGF and PIGF binding, preventing the interaction between VEGF/PIGF and VEGFR1/2. 19 Investigators have found that the activation of Notch1 and Hes1 can promote angiogenesis and vascular endothelial cell injury repair. 20,21 Consistently, our previous studies have also suggested that Notch1 promotes VEGF-mediated angiogenesis and inhibits myocardial interstitial fibrosis.…”

Section: Discussionmentioning

confidence: 99%

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Inhibition of the Notch1 pathway induces peripartum cardiomyopathy

Zhu

Chen

Liu

et al. 2020

J Cellular Molecular Medi

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Increased expression and activity of cardiac and circulating cathepsin D and soluble fms‐like tyrosine kinase‐1 (sFlt‐1) have been demonstrated to induce and promote peripartum cardiomyopathy (PPCM) via promoting cleavage of 23‐kD prolactin (PRL) to 16‐kD PRL and neutralizing vascular endothelial growth factor (VEGF), respectively. We hypothesized that activation of Hes1 is proposed to suppress cathepsin D via activating Stat3, leading to alleviated development of PPCM. In the present study, we aimed to investigate the role of Notch1/Hes1 pathway in PPCM. Pregnant mice between prenatal 3 days and postpartum 3 weeks were fed with LY‐411575 (a notch inhibitor, 10 mg/kg/d). Ventricular function and pathology were evaluated by echocardiography and histological analysis. Western blotting analysis was used to examine the expression at the protein level. The results found that inhibition of Notch1 significantly promoted postpartum ventricular dilatation, myocardial hypertrophy and myocardial interstitial fibrosis and suppressed myocardial angiogenesis. Western blotting analysis showed that inhibition of Notch1 markedly increased cathepsin D and sFlt‐1, reduced Hes1, phosphorylated Stat3 (p‐Stat3), VEGFA and PDGFB, and promoted cleavage of 23k‐D PRL to 16‐kD PRL. Collectively, inhibition of Notch1/Hes1 pathway induced and promoted PPCM via increasing the expressions of cathepsin D and sFlt‐1. Notch1/Hes1 was a promising target for prevention and therapeutic regimen of PPCM.

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Section: Discussionmentioning

confidence: 99%