ArticleCell death & disease2019
Oocyte-derived E-cadherin acts as a multiple functional factor maintaining the primordial follicle pool in mice.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 42 citations in OpenAlex.
- Physical activity delays ovarian aging in part through adiponectin-related signaling pathways.Nature aging · 2026Article
- MicroRNA expression profiling and functional analysis of CDH3 during oogenesis in the Chinese alligator (Current zoology · 2026Article
- Gene regulatory networks orchestrating oocyte fate bifurcation in primordial follicles revealed by single-cell transcriptomics.Communications biology · 2026Article
- Maternal sleep deprivation during pregnancy induced offspring germ cells loss through ferroptosis.Cell death discovery · 2025Article
- CCAAT/enhancer binding protein beta (C/EBPβ) regulates the formation of the ovarian reserve.Communications biology · 2025Article
- Luteinizing Hormone Preserves Oocyte-Granulosa Cell Communication in Growing Follicles Exposed to Chemotherapy with Alkylating Agents at the Primordial Stage in a Mouse Model.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- Genetic insights into the complexity of premature ovarian insufficiency.Reproductive biology and endocrinology : RB&E · 2024Review
- DNA methylation, but not microRNA expression, is affected by in vitro THC exposure in bovine granulosa cells.BMC pharmacology & toxicology · 2024Article
- HDAC6-dependent deacetylation of NGF dictates its ubiquitination and maintains primordial follicle dormancy.Theranostics · 2024Article
- ROCK1 is a multifunctional factor maintaining the primordial follicle reserve and follicular development in mice.American journal of physiology. Cell physiology · 2024Article
- cAMP controls the balance between dormancy and activation of primordial follicles in mouse ovaries.PNAS nexus · 2023Article
- The metallic compound promotes primordial follicle activation and ameliorates fertility deficits in aged mice.Theranostics · 2023Article
- Mechanisms of primordial follicle activation and new pregnancy opportunity for premature ovarian failure patients.Frontiers in physiology · 2023Review
- Review
- hnRNPH1 recruits PTBP2 and SRSF3 to modulate alternative splicing in germ cells.Nature communications · 2022Article
- Regulation of mouse primordial follicle formation by signaling through the PI3K pathway†.Biology of reproduction · 2022Article
- Enhanced glycolysis in granulosa cells promotes the activation of primordial follicles through mTOR signaling.Cell death & disease · 2022Article
- Article
- Transcriptomic Profile of New Gene Markers Encoding Proteins Responsible for Structure of Porcine Ovarian Granulosa Cells.Biology · 2021Article
- Primordial Follicle Formation - Some Assembly Required.Current opinion in endocrine and metabolic research · 2021Article
Corrections and comments
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In mammals, female fecundity is determined by the size of the primordial follicle (PF) pool, which is established during the perinatal period. As a non-renewable resource, the preservation of dormant PFs is crucial for sustaining female reproduction throughout life. Although studies have revealed that several oocyte-derived functional genes and pathways, such as newborn ovary homeobox (NOBOX) and 3-phosphoinositide-dependent protein kinase-1, participate in maintaining the PF pool, our understanding of the underlying molecular mechanisms is still incomplete. Here, we demonstrate that E-cadherin (E-cad) plays a crucial role in the maintenance of PFs in mice. E-cad is specifically localized to the cytomembrane of oocytes in PFs. Knockdown of E-cad in neonatal ovaries resulted in significant PF loss owing to oocyte apoptosis. In addition, the expression pattern of NOBOX is similar to that of E-cad. Knockdown of E-cad resulted in a decreased NOBOX level, whereas overexpression of Nobox partially rescued the follicle loss induced by silencing E-cad. Furthermore, E-cad governed NOBOX expression by regulating the shuttle protein, β-catenin, which acts as a transcriptional co-activator. Notably, E-cad, which is a transmembrane protein expressed in the oocytes, was also responsible for maintaining the PF structure by facilitating cell-cell adhesive contacts with surrounding pregranulosa cells. In conclusion, E-cad in oocytes of PFs plays an indispensable role in the maintenance of the PF pool by facilitating follicular structural stability and regulating NOBOX expression. These findings shed light on the physiology of sustaining female reproduction.
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