Placental extracellular vesicles promote cardiomyocyte maturation and fetal heart development

Congenital heart defects are leading causes of neonatal mortality and are often associated with placental abnormalities, but mechanisms linking placenta and heart development are poorly understood. Herein, we investigated a potential signaling network connecting the placenta and nascent heart in mice. We found that fetal hearts exposed to media conditioned by placental tissue or differentiated wild-type trophoblast stem (TS) cells, but not undifferentiated TS cells, showed increased heart rate and epicardial cell outgrowth. This effect was not observed when hearts were exposed to media from TS cells lacking OVO-Like 2, a transcription factor required for trophoblast differentiation and placental development. Trophoblasts released abundant extracellular vesicles into media, and these vesicles were sufficient to mediate cardio-promoting effects. Our findings provide a potential mechanism whereby the placenta communicates with the fetal heart to promote cardiac morphogenesis, and offers insight into the link between poor placentation and a higher incidence of heart defects.

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Publication Details

Journal
Communications Biology
Published
2024-10-03
DOI
https://doi.org/10.1038/s42003-024-06938-4
Citations
10
Primary Topic
Pregnancy and preeclampsia studies
Type
article
Field-Weighted Citation Impact
5.24

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Placental extracellular vesicles promote cardiomyocyte maturation and fetal heart development

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article

Placental extracellular vesicles promote cardiomyocyte maturation and fetal heart development

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article en
10 citations

Abstract

Congenital heart defects are leading causes of neonatal mortality and are often associated with placental abnormalities, but mechanisms linking placenta and heart development are poorly understood. Herein, we investigated a potential signaling network connecting the placenta and nascent heart in mice. We found that fetal hearts exposed to media conditioned by placental tissue or differentiated wild-type trophoblast stem (TS) cells, but not undifferentiated TS cells, showed increased heart rate and epicardial cell outgrowth. This effect was not observed when hearts were exposed to media from TS cells lacking OVO-Like 2, a transcription factor required for trophoblast differentiation and placental development. Trophoblasts released abundant extracellular vesicles into media, and these vesicles were sufficient to mediate cardio-promoting effects. Our findings provide a potential mechanism whereby the placenta communicates with the fetal heart to promote cardiac morphogenesis, and offers insight into the link between poor placentation and a higher incidence of heart defects.

Communications BiologyVol. 7(1)
Western University (CA), Children’s Health Research Institute (CA)
Children's Health Research Institute, Canadian Institutes of Health Research, Natural Sciences and Engineering Research Council of Canada
Zero hunger
Openalex Percentile: Top 4%
Pregnancy and preeclampsia studies
5.24
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