ArticleProceedings of the National Academy of Sciences of the United States of America2020
Atypical protein kinase C iota (PKCλ/ι) ensures mammalian development by establishing the maternal-fetal exchange interface.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 23 citations in OpenAlex.
- An Integrated Proteomics and Genomics Approach to Identify Essential Protein Kinases During Human Trophoblast Development.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- The Role of Branched-Chain Amino Acids in Nutrient Allocation of the Porcine Placenta: A Review.Animals : an open access journal from MDPI · 2026Review
- aPKC-ζ III promotes trophoblast fusion by altering Par-3 interactions with Hippo signaling kinase LATS1.Stem cell reports · 2026Article
- Arginine methyltransferase PRMT1 equipoises trophoblast development to prevent early pregnancy loss.Nature communications · 2026Article
- Functional heterogeneity in trophoblast stem cells derived from recurrent pregnancy loss products of conception.Molecular human reproduction · 2026Article
- Prkci acts a pro-proliferation factor in colorectal cancer.NPJ precision oncology · 2025Article
- Two classes of syncytiotrophoblast nuclei form following BAP-driven human pluripotent stem cell differentiation.Placenta · 2025Article
- Leveraging chorionic villus biopsies for the derivation of patient-specific trophoblast stem cells.Communications biology · 2025Article
- FXYD1 was identified as a hub gene in recurrent miscarriage and involved in decidualization via regulating Na/K-ATPase activity.Journal of assisted reproduction and genetics · 2025Article
- Epigenetic dynamics of partially methylated domains in human placenta and trophoblast stem cells.BMC genomics · 2024Article
- Downregulation of PRKCI inhibits osteosarcoma cell growth by inactivating the Akt/mTOR signaling pathway.Frontiers in oncology · 2024Article
- Loss of polarity regulators initiates gasdermin-E-mediated pyroptosis in syncytiotrophoblasts.Life science alliance · 2023Article
- Dual contribution of the mTOR pathway and of the metabolism of amino acids in prostate cancer.Cellular oncology (Dordrecht, Netherlands) · 2022Review
- Hippo signaling cofactor, WWTR1, at the crossroads of human trophoblast progenitor self-renewal and differentiation.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- How trophoblasts fuse: an in-depth look into placental syncytiotrophoblast formation.Cellular and molecular life sciences : CMLS · 2022Review
- Paradigms for investigating invasive trophoblast cell development and contributions to uterine spiral artery remodeling.Placenta · 2021Review
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
Abstract
In utero mammalian development relies on the establishment of the maternal-fetal exchange interface, which ensures transportation of nutrients and gases between the mother and the fetus. This exchange interface is established via development of multinucleated syncytiotrophoblast cells (SynTs) during placentation. In mice, SynTs develop via differentiation of the trophoblast stem cell-like progenitor cells (TSPCs) of the placenta primordium, and in humans, SynTs are developed via differentiation of villous cytotrophoblast (CTB) progenitors. Despite the critical need in pregnancy progression, conserved signaling mechanisms that ensure SynT development are poorly understood. Herein, we show that atypical protein kinase C iota (PKCλ/ι) plays an essential role in establishing the SynT differentiation program in trophoblast progenitors. Loss of PKCλ/ι in the mouse TSPCs abrogates SynT development, leading to embryonic death at approximately embryonic day 9.0 (E9.0). We also show that PKCλ/ι-mediated priming of trophoblast progenitors for SynT differentiation is a conserved event during human placentation. PKCλ/ι is selectively expressed in the first-trimester CTBs of a developing human placenta. Furthermore, loss of PKCλ/ι in CTB-derived human trophoblast stem cells (human TSCs) impairs their SynT differentiation potential both in vitro and after transplantation in immunocompromised mice. Our mechanistic analyses indicate that PKCλ/ι signaling maintains expression of GCM1, GATA2, and PPARγ, which are key transcription factors to instigate SynT differentiation programs in both mouse and human trophoblast progenitors. Our study uncovers a conserved molecular mechanism, in which PKCλ/ι signaling regulates establishment of the maternal-fetal exchange surface by promoting trophoblast progenitor-to-SynT transition during placentation.
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