ArticleMolecular endocrinology (Baltimore, Md.)2011
CCAAT/enhancer-binding proteins (C/EBP)-α and -β are essential for ovulation, luteinization, and the expression of key target genes.
Article in Molecular endocrinology (Baltimore, Md.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.
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77 citing papers in PubMed, 168 citations in OpenAlex.
- Moving Beyond Somatic Alterations: Uncovering the Germline Basis of Myeloid Malignancies.Cancers · 2026Review
- Identification and Functional Analysis ofBiomolecules · 2026Article
- Doppler Ultrasonography for Live Imaging and Quantification of Ovarian Vascular Function in Mice.Journal of visualized experiments : JoVE · 2025Article
- CCAAT/enhancer binding protein beta (C/EBPβ) regulates the formation of the ovarian reserve.Communications biology · 2025Article
- Semaphorin 3E-Plexin-D1 Pathway Downstream of the Luteinizing Hormone Surge Regulates Ovulation, Granulosa Cell Luteinization, and Ovarian Angiogenesis in Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The roles of MAPK signaling pathway in ovarian folliculogenesis.Journal of ovarian research · 2025Review
- Hyperandrogen-induced imbalance of FOXO4-AR regulatory loop contributes to ovulatory disorders in polycystic ovary syndrome.Molecular therapy. Nucleic acids · 2025Article
- CCAAT/Enhancer-Binding Proteins α and β Regulate Ovulation and Gene Expression via Dose- and Stage-Dependent Mechanisms.Endocrinology · 2025Article
- Downregulation of FASN in granulosa cells and its impact on ovulatory dysfunction in PCOS.Journal of ovarian research · 2025Article
- Characterizing the Role of Endocannabinoid Receptor Cnr1 in Mouse Ovarian Granulosa Cells.Cell biochemistry and function · 2025Article
- Granulosa cell expression of Fos is critical for regulating ovulatory gene expressions in the mouse ovary.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Heterozygous Eif4nif1 Stop-Gain Mice Replicate the Primary Ovarian Insufficiency Phenotype in Women.Endocrinology · 2025Article
- New insights into the ovulatory process in the human ovary.Human reproduction update · 2025Review
- Single-cell sequencing reveals transcriptional dynamics regulated by ERα in mouse ovaries.PloS one · 2024Article
- Article
- ERK1/2-SOX9/FOXL2 axis regulates ovarian steroidogenesis and favors the follicular-luteal transition.Life science alliance · 2023Article
- Progesterone receptor mediates ovulatory transcription through RUNX transcription factor interactions and chromatin remodelling.Nucleic acids research · 2023Article
- Ovulatory signal-triggered chromatin remodeling in ovarian granulosa cells by HDAC2 phosphorylation activation-mediated histone deacetylation.Epigenetics & chromatin · 2023Article
- MitoQ Protects Ovarian Organoids against Oxidative Stress during Oogenesis and Folliculogenesis In Vitro.International journal of molecular sciences · 2023Article
- Decreased Expression of EZH2 in Granulosa Cells Contributes to Endometriosis-Associated Infertility by Targeting IL-1R2.Endocrinology · 2022Article
17 more citing papers are in PubMed but not listed here.
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4 authors at 2 institutions in 1 country.
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Abstract
LH activation of the epidermal growth factor receptor/RAS/ERK1/2 pathway is essential for ovulation and luteinization because granulosa cell (GC) depletion of ERK1/2 (ERK1/2(gc)(-/-) mice) renders mice infertile. As mediators of ERK1/2-dependent GC differentiation, the CCAAT/enhancer-binding proteins, (C/EBP)α and C/EBPβ, were also disrupted. Female Cebpb(gc)(-/-) mutant mice, but not Cebpa(gc)(-/-) mice, were subfertile whereas Cebpa/b(gc)(-/-) double-mutant females were sterile. Follicles failed to ovulate, ovaries were devoid of corpora lutea, luteal cell marker genes (Lhcgr, Prlr, Ptgfr, Cyp11a1, and Star) were absent, and serum progesterone levels were low. Microarray analyses identified numerous C/EBPα/β target genes in equine chorionic gonadotropin (eCG)-human (h)CG-treated mice. At 4 h post-hCG, a subset (19%) of genes altered in the Cebpa/b-depleted cells was also altered in ERK1/2-depleted cells; hence they are common effectors of ERK1/2. Additional genes down-regulated in the Cebpa/b-depleted cells at 8 and 24 h post-hCG include known (Akr1b7, Runx2, Star, Saa3) and novel (Abcb1b, Apln, Igfbp4, Prlr, Ptgfr Timp4) C/EBP targets and effectors of luteal and vascular cell development. Bhmt, a gene controlling methionine metabolism and thought to be expressed exclusively in liver and kidney, was high in wild-type luteal cells but totally absent in Cebpa/b mutant cells. Because numerous genes potentially associated with vascular development were suppressed in the mutant cells, C/EBPα/β appear to dictate the luteinization process by also controlling genes that regulate the formation of the extensive vascular network required to sustain luteal cells. Thus, C/EBPα/β mediate the terminal differentiation of GCs during the complex process of luteinization.
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