4.7 Article

Single-cell transcriptional profiling reveals cellular and molecular divergence in human maternal-fetal interface

Journal

SCIENTIFIC REPORTS
Volume 12, Issue 1, Pages -

Publisher

NATURE PORTFOLIO
DOI: 10.1038/s41598-022-14516-z

Keywords

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Funding

  1. China National GeneBank
  2. Science, Technology and Innovation Commission of Shenzhen Municipality Grant [JCYJ20180507183628543]

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This study surveyed the single-cell transcriptomic landscape of human full-term placenta, revealing the heterogeneity of cytotrophoblast cell and stromal cell, and identified a subpopulation of CTB called trophoblast progenitor-like cells. Furthermore, a key transcription factor that may promote enEVT cell differentiation was identified.
Placenta plays essential role in successful pregnancy, as the most important organ connecting and interplaying between mother and fetus. However, the cellular characteristics and molecular interaction of cell populations within the fetomaternal interface is still poorly understood. Here, we surveyed the single-cell transcriptomic landscape of human full-term placenta and revealed the heterogeneity of cytotrophoblast cell (CTB) and stromal cell (STR) with the fetal/maternal origin consecutively localized from fetal section (FS), middle section (Mid_S) to maternal section (Mat_S) of maternal-fetal interface. Then, we highlighted a subpopulation of CTB, named trophoblast progenitor-like cells (TPLCs) existed in the full-term placenta and mainly distributed in Mid_S, with high expression of a pool of putative cell surface markers. Further, we revealed the putative key transcription factor PRDM6 that might promote the differentiation of endovascular extravillous trophoblast cells (enEVT) by inhibiting cell proliferation, and down-regulation of PRDM6 might lead to an abnormal enEVT differentiation process in PE. Together, our study offers important resources for better understanding of human placenta and stem cell-based therapy, and provides new insights on the study of tissue heterogeneity, the clinical prevention and control of PE as well as the maternal-fetal interface.

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