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Increasing heart vascularisation after myocardial infarction using brain natriuretic peptide stimulation of endothelial and WT1⁺ epicardial cells.

ABSTRACT: Brain natriuretic peptide (BNP) treatment increases heart function and decreases heart dilation after myocardial infarction (MI). Here, we investigated whether part of the cardioprotective effect of BNP in infarcted hearts related to improved neovascularisation. Infarcted mice were treated with saline or BNP for 10 days. BNP treatment increased vascularisation and the number of endothelial cells in all areas of infarcted hearts. Endothelial cell lineage tracing showed that BNP directly stimulated the proliferation of resident endothelial cells via NPR-A binding and p38 MAP kinase activation. BNP also stimulated the proliferation of WT1⁺ epicardium-derived cells but only in the hypoxic area of infarcted hearts. Our results demonstrated that these immature cells have a natural capacity to differentiate into endothelial cells in infarcted hearts. BNP treatment increased their proliferation but not their differentiation capacity. We identified new roles for BNP that hold potential for new therapeutic strategies to improve recovery and clinical outcome after MI.

SUBMITTER: Li N

PROVIDER: S-EPMC7695454 | biostudies-literature | 2020 Nov

REPOSITORIES: biostudies-literature

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Increasing heart vascularisation after myocardial infarction using brain natriuretic peptide stimulation of endothelial and WT1<sup>+</sup> epicardial cells.

Li Na N Rignault-Clerc Stephanie S Bielmann Christelle C Bon-Mathier Anne-Charlotte AC Déglise Tamara T Carboni Alexia A Ducrest Mégane M Rosenblatt-Velin Nathalie N

eLife 20201127

Brain natriuretic peptide (BNP) treatment increases heart function and decreases heart dilation after myocardial infarction (MI). Here, we investigated whether part of the cardioprotective effect of BNP in infarcted hearts related to improved neovascularisation. Infarcted mice were treated with saline or BNP for 10 days. BNP treatment increased vascularisation and the number of endothelial cells in all areas of infarcted hearts. Endothelial cell lineage tracing showed that BNP directly stimulate ...[more]

PMID: 33245046

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Project description:ObjectiveTo determine the predictive value of pro-C-type natriuretic peptide (pro-CNP) measurement in plasma sampled on admission from patients presenting with ST-elevation myocardial infarction (STEMI).DesignProspective cohort study.SettingTwo University Hospitals in Denmark.Participants1760 consecutive patients (470 females and 1290 males) with confirmed STEMI.Main outcomes and measuresThe main outcome was all-cause mortality at 1 year after presentation and the primary measure was pro-CNP concentration in plasma at admission in all patients and longitudinal measurements in a consecutive subgroup of 287 patients. A reference population (n=688) defined cut-off values of increased pro-CNP concentrations.ResultsIn all patients, an increased pro-CNP concentration was associated with a higher all-cause mortality after 1 year (HR 1.6, 95% CI 1.1 to 2.4, Plogrank=0.009) including an interaction of sex (p=0.03). In separate sex-stratified analyses, female patients showed increased all-cause mortality (HR1 year 2.6, 95% CI 1.5 to 4.6), Plogrank <0.001), whereas no differences were found in male patients (HR1 year 1.1, 95% CI 0.7 to 1.9, Plogrank=0.66). After adjusting for potential risk factors, we found increased pro-CNP concentrations≥the median value to be independently associated with increased risk of mortality in female patients within 1 year (HR per 1 pmol/L increase: 1.04, 95% CI 1.01 to 1.06, p=0.007). Moreover, we found indications of sex differences in pro-CNP concentrations over time (higher pro-CNP in males (4.4, 95% CI -0.28 to 9.1 pmol/L, p=0.07) and interaction of sex and time (p=0.13)), and that hypertension was independently associated with higher pro-CNP (4.5, 95% CI 0.6 to 8.4 pmol/L, p=0.03).ConclusionsIn female but not male patients presenting with STEMI, high concentrations of pro-CNP (≥median) at admission independently indicate a higher risk of all-cause mortality. The findings are remarkably specific for female patients, suggesting a different vascular phenotype beyond traditional measures of coronary artery flow compared with male patients.

Dataset Information

Increasing heart vascularisation after myocardial infarction using brain natriuretic peptide stimulation of endothelial and WT1⁺ epicardial cells.

Publications

Increasing heart vascularisation after myocardial infarction using brain natriuretic peptide stimulation of endothelial and WT1<sup>+</sup> epicardial cells.

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Dataset Information

Increasing heart vascularisation after myocardial infarction using brain natriuretic peptide stimulation of endothelial and WT1+ epicardial cells.

Publications

Increasing heart vascularisation after myocardial infarction using brain natriuretic peptide stimulation of endothelial and WT1<sup>+</sup> epicardial cells.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets

Increasing heart vascularisation after myocardial infarction using brain natriuretic peptide stimulation of endothelial and WT1⁺ epicardial cells.