ArticleCell death discovery2024
Identification of apelin/APJ signaling dysregulation in a human iPSC-derived granulosa cell model of Turner syndrome.
Article in Cell death discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
5 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Sex chromosome aneuploidy impacts on human gene expression and regulation: a systematic review.Molecular medicine (Cambridge, Mass.) · 2025Pooled it
- Expression of New Gene Markers Regulating Protein Metabolism in Porcine Ovarian Granulosa Cells In Vitro.International journal of molecular sciences · 2025Article
- Derivation of Granulosa-Like Cells from Human Endometrial iPSCs for Autologous Estradiol Production.Tissue engineering and regenerative medicine · 2025Article
- Dissection of the gene regulatory network underlying sexual maturity divergence in Jining Bairi chickens through integrated RNA-seq and WGCNA analysis.Poultry science · 2025Article
- APJ regulates the balance between self-renewal and differentiation of vascular endothelial stem cells.Inflammation and regeneration · 2025Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
The interaction between germ cells and somatic cells in the ovaries plays a crucial role in establishing the follicle reserve in mammals. Turner syndrome (TS) predominantly affects females who have a partial or complete loss of one X chromosome. Our understanding of the role that granulosa cells (GCs) play in TS disease progression and pathogenesis remains limited. In this study, we achieved GC differentiation efficiency of up to 80% from iPSCs. When attempting to replicate the differentiation process of embryonic granulosa cells, we observed the downregulation of specific genes-GATA4, FOXL2, AMHR2, CYP19A1, and FSH-in Turner syndrome-derived granulosa cells (TS-GCs). Additionally, we identified dysregulation of the cell cycle in TS-GCs. To uncover the endogenous defects in TS-GCs, we compared global transcriptome patterns between iPSC-derived granulosa cells from healthy individuals and those with Turner syndrome. The apelin/APJ pathway exhibited differential signaling between the healthy and TS groups. Supplementation with apelin ligands and activation of apelin/APJ downstream signaling via Akt/PKB restored cell cycle progression and marker gene expression. We hypothesize that during early embryonic development, failures in apelin/APJ signaling in GCs of Turner syndrome patients lead to abnormalities in ovarian development, ultimately resulting in early oocyte loss and infertility.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.