ArticleScientific reports2023
Mitochondrial citrate metabolism and efflux regulate BeWo differentiation.
Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Metabolism and homeostasis of energy in trophoblast cells of the placenta: from development to disease†.Biology of reproduction · 2026Review
- Placental mitochondrial calcium uniporter modulates offspring susceptibility to metabolic dysfunction.Molecular metabolism · 2025Article
- The oxygen level in air directs airway epithelial cell differentiation by controlling mitochondrial citrate export.Science advances · 2025Article
- Multi-omics analysis reveals a protective role of endogenous proline in sheep oocyte vitrification and its therapeutic application.Frontiers in cell and developmental biology · 2025Article
- TFEB safeguards trophoblast syncytialization in humans and mice.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
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13 authors at 3 institutions in 1 country.
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Abstract
Cytotrophoblasts fuse to form and renew syncytiotrophoblasts necessary to maintain placental health throughout gestation. During cytotrophoblast to syncytiotrophoblast differentiation, cells undergo regulated metabolic and transcriptional reprogramming. Mitochondria play a critical role in differentiation events in cellular systems, thus we hypothesized that mitochondrial metabolism played a central role in trophoblast differentiation. In this work, we employed static and stable isotope tracing untargeted metabolomics methods along with gene expression and histone acetylation studies in an established BeWo cell culture model of trophoblast differentiation. Differentiation was associated with increased abundance of the TCA cycle intermediates citrate and α-ketoglutarate. Citrate was preferentially exported from mitochondria in the undifferentiated state but was retained to a larger extent within mitochondria upon differentiation. Correspondingly, differentiation was associated with decreased expression of the mitochondrial citrate transporter (CIC). CRISPR/Cas9 disruption of the mitochondrial citrate carrier showed that CIC is required for biochemical differentiation of trophoblasts. Loss of CIC resulted in broad alterations in gene expression and histone acetylation. These gene expression changes were partially rescued through acetate supplementation. Taken together, these results highlight a central role for mitochondrial citrate metabolism in orchestrating histone acetylation and gene expression during trophoblast differentiation.
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