Why the study?
BNP improves heart function and reduces dilation after MI, but whether this cardioprotection relates to improved neovascularisation remained unclear.
Does brain natriuretic peptide improve neovascularisation in infarcted mice?
Does brain natriuretic peptide improve neovascularisation in infarcted mice?
BNP treatment promotes neovascularisation after myocardial infarction by stimulating the proliferation of resident mature endothelial cells and WT1+ epicardium-derived cells.
Brain natriuretic peptide (BNP) treatment increases heart function and decreases heart dilation after myocardial infarction. 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 the infarct border and remote zones of infarcted hearts. Endothelial cell lineage tracing showed that BNP directly stimulated the proliferation of resident mature endothelial cells in both areas of the infarcted hearts, 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 and new therapeutic strategies to improve heart recovery in infarcted hearts.
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Li et al. (2020) studied this question.
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