Involvement of atypical transcription factor E2F8 in the polyploidization during mouse and human decidualization
Open accessAbstract
Polyploid decidual cells are specifically differentiated cells during mouse uterine decidualization. However, little is known about the regulatory mechanism and physiological significance of polyploidization in pregnancy. Here we report a novel role of E2F8 in the polyploidization of decidual cells in mice. E2F8 is highly expressed in decidual cells and regulated by progesterone through HB-EGF/EGFR/ERK/STAT3 signaling pathway. E2F8 transcriptionally suppresses CDK1, thus triggering the polyploidization of decidual cells. E2F8-mediated polyploidization is a response to stresses which are accompanied by decidualization. Interestingly, polyploidization is not detected during human decidualization with the down-regulation of E2F8, indicating differential expression of E2F8 may lead to the difference of decidual cell polyploidization between mice and humans.
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E2f7 and E2f8 are expressed in several other tissues, such as placenta and pancreas, where they are implicated in arresting the cell cycle.
“These mitotic inhibitors are expressed in several other tissues, such as the placenta and pancreas, where they are also implicated in arresting the cell cycle (8, 47–49).”
From Wnt signaling regulates hepatocyte cell division by a transcriptional repressor cascade (2022) · cites this paper as [47]
The Introduction (page not provided) links E2F7 and E2F8 to trophoblast giant cells and describes them as transcriptional repressors. The section “E2F8 initiates the endoreplication of mouse decidual cells” (page not provided) says E2F8 represses mitosis and cytokinesis in decidual cells. Our copy does not establish expression in the pancreas or cell-cycle arrest in the placenta and pancreas. (LLM, conf=0.84)
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“Additionally, E2F8 was detected in decidual cells, as previously reported (17).”
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“Additionally, in human ectopic endome ‐ triotic lesions, FGF9, which is stimulated by estrogen of endometriotic stromal cell origin, regulates the pro ‐ liferation of endometriotic stromal cells in an auto ‐ crine manner (Zhao et al., 2015).”
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- Authors
- Qi, Q.-R., Zhao, X.-Y., Zuo, R.-J., Wang, T.-S., Gu, X.-W., Liu, J.-L., & Yang, Z.-M.
- Affiliations
- South China Agricultural University (CN)
- Shantou University (CN)
- Department of Biology; Shantou University; Shantou, China
- College of Veterinary Medicine; South China Agricultural University; Guangzhou, China
- Corresponding author
- Yang, Zeng-Ming
- Venue
- Cell Cycle
- Publisher
- Informa UK Limited
- Published
- 2015-06-17
- Volume
- 14
- Issue
- 12
- Pages
- 1842-1858
- ISSN
- 1538-4101 (ISSN-L)
- 1551-4005
- PMC
- PMC4614110
- OpenAlex
- W1605876551
- Cited by
- 58
- References
- 47
- Citations by year
- 2026: 3 · 2025: 6 · 2024: 6 · 2023: 4 · 2022: 6 · 2021: 8 · 2020: 8 · 2019: 3 · 2018: 6 · 2017: 2 · 2016: 4 · 2015: 2
- FWCI
- 2.30
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Cell Cycle (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (31271602, 31471397, 31272263)
- National Key Research and Development Program of China (2013CB910803, 2011CB944402)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Reproductive System and Pregnancy
- Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy and preeclampsia studies
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
- Keywords
- E2F8, polyploidization, uterine decidualization, decidual cells, CDK1, progesterone signaling, transcriptional regulation, pregnancy
- MeSH terms
- Animals, Cell Line, Decidua, DNA Damage, Female, Flow Cytometry, Humans, Microscopy, Fluorescence, Ovary, Polyploidy, Pregnancy, Pregnancy, Animal, Progesterone, Repressor Proteins, Superoxide Dismutase, Uterus, Signal Transduction, CDC2 Protein Kinase, Cyclin-Dependent Kinases, Hepatocytes, Mice
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