ArticleEndocrinology2016
Progesterone-Dependent Induction of Phospholipase C-Related Catalytically Inactive Protein 1 (PRIP-1) in Decidualizing Human Endometrial Stromal Cells.
Article in Endocrinology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
17 citing papers in PubMed, 39 citations in OpenAlex.
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- Assessment of the histone mark-based epigenomic landscape in human myometrium at term pregnancy.eLife · 2025Article
- Deciphering the role of rapamycin in modulating decidual senescence: implications for decidual remodeling and implantation failure.Journal of assisted reproduction and genetics · 2024Article
- An integrated single-cell reference atlas of the human endometrium.Nature genetics · 2024Article
- Identification of Potentially Novel Molecular Targets of Endometrial Cancer Using a Non-Biased Proteomic Approach.Cancers · 2023Article
- The effects of progesterone on immune cellular function at the maternal-fetal interface and in maternal circulation.The Journal of steroid biochemistry and molecular biology · 2023Review
- Progesterone receptor isoform B regulates theProceedings of the National Academy of Sciences of the United States of America · 2021Article
- The Role of Decidual Subpopulations in Implantation, Menstruation and Miscarriage.Frontiers in reproductive health · 2021Review
- Exometabolomic Analysis of Decidualizing Human Endometrial Stromal and Perivascular Cells.Frontiers in cell and developmental biology · 2021Article
- Endometrial Decidualization: The Primary Driver of Pregnancy Health.International journal of molecular sciences · 2020Review
- Dynamic transcriptome, accessible genome, and PGR cistrome profiles in the human myometrium.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Recurrent pregnancy loss is associated with a pro-senescent decidual response during the peri-implantation window.Communications biology · 2020Article
- Vascular Adhesion Protein-1 Determines the Cellular Properties of Endometrial Pericytes.Frontiers in cell and developmental biology · 2020Article
- Tumor Cell "Slimming" Regulates Tumor Progression through PLCL1/UCP1-Mediated Lipid Browning.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2019Article
- Resveratrol inhibits decidualization by accelerating downregulation of the CRABP2-RAR pathway in differentiating human endometrial stromal cells.Cell death & disease · 2019Article
- Analysis of chromatin accessibility in decidualizing human endometrial stromal cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- LEFTY2 inhibits endometrial receptivity by downregulating Orai1 expression and store-operated CaJournal of molecular medicine (Berlin, Germany) · 2018Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Decidualization denotes the transformation of endometrial stromal cells into specialized decidual cells. In pregnancy, decidual cells form a protective matrix around the implanting embryo, enabling coordinated trophoblast invasion and formation of a functional placenta. Continuous progesterone (P4) signaling renders decidual cells resistant to various environmental stressors, whereas withdrawal inevitably triggers tissue breakdown and menstruation or miscarriage. Here, we show that PLCL1, coding phospholipase C (PLC)-related catalytically inactive protein 1 (PRIP-1), is highly induced in response to P4 signaling in decidualizing human endometrial stromal cells (HESCs). Knockdown experiments in undifferentiated HESCs revealed that PRIP-1 maintains basal phosphoinositide 3-kinase/Protein kinase B activity, which in turn prevents illicit nuclear translocation of the transcription factor forkhead box protein O1 and induction of the apoptotic activator BIM. By contrast, loss of this scaffold protein did not compromise survival of decidual cells. PRIP-1 knockdown did also not interfere with the responsiveness of HESCs to deciduogenic cues, although the overall expression of differentiation markers, such as PRL, IGFBP1, and WNT4, was blunted. Finally, we show that PRIP-1 in decidual cells uncouples PLC activation from intracellular Ca(2+) release by attenuating inositol 1,4,5-trisphosphate signaling. In summary, PRIP-1 is a multifaceted P4-inducible scaffold protein that gates the activity of major signal transduction pathways in the endometrium. It prevents apoptosis of proliferating stromal cells and contributes to the relative autonomy of decidual cells by silencing PLC signaling downstream of Gq protein-coupled receptors.
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