ArticleReproductive biology and endocrinology : RB&E2022
Down-regulation of PBK inhibits proliferation of human endometrial stromal cells in thin endometrium.
Article in Reproductive biology and endocrinology : RB&E, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 24 citations in OpenAlex.
- GM-CSF improves the receptivity of thin endometrium by promoting glandular and stromal cell proliferation in mice and humans.Cell death discovery · 2025Article
- Targeting PBK with small-molecule 1-Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Identification and Validation of RPL7 and RCCD1 as Potential Biomarkers Associated with Immune Infiltration in Patients with Thin Endometrium.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- Thermo-sensitive ε-polylysine-heparin-poloxamer hydrogel-encapsulated BMSCs promote endometrial regeneration.Materials today. Bio · 2025Article
- Advances in using biomaterials for repairing thin endometrium.Frontiers in bioengineering and biotechnology · 2025Review
- Establishment and validation of the prognostic risk model based on the anoikis-related genes in esophageal squamous cell carcinoma.Annals of medicine · 2024Article
- Altered Expressions ofJournal of clinical medicine · 2024Article
- Altered Expression ofDiagnostics (Basel, Switzerland) · 2024Article
- PBK correlates with prognosis, immune escape and drug response in LUAD.Scientific reports · 2023Article
- Quantitative Proteomic Analysis of Zearalenone-Induced Intestinal Damage in Weaned Piglets.Toxins · 2022Article
- Network Pharmacology and Molecular Docking Approach to Reveal the Immunotherapeutic Mechanism of Cuscutae Semen in Treating Thin Endometrium.Journal of immunology research · 2022Article
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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
backgroundThin endometrium (TE) is a challenging clinical issue in the reproductive medicine characterized by inadequate endometrial thickness, poor response to estrogen and no effective treatments currently. At present, the precise pathogenesis of thin endometria remains to be elucidated. We aimed to explore the related molecular mechanism of TE by comparing the transcriptome profiles of late-proliferative phase endometria between TE and matched controls.
methodsWe performed a bulk RNA-Seq (RNA-sequencing) of endometrial tissues in the late-proliferative phase in 7 TE and 7 matched controls for the first time. Differential gene expression analysis, gene ontology enrichment analysis and protein-protein interactions (PPIs) network analysis were performed. Immunohistochemistry was used for molecular expression and localization in endometria. Human endometrial stromal cells (HESCs) were isolated and cultured for verifying the functions of hub gene.
resultsIntegrative data mining of our RNA-seq data in endometria revealed that most genes related to cell division and cell cycle were significantly inhibited, while inflammation activation, immune response and reactive oxygen species associated genes were upregulated in TE. PBK was identified as a hub of PPIs network, and its expression level was decreased by 2.43-fold in endometria of TE patients, particularly reduced in the stromal cells, which was paralleled by the decreased expression of Ki67. In vitro experiments showed that the depletion of PBK reduced the proliferation of HESCs by 50% and increased the apoptosis of HESCs by 1 time, meanwhile PBK expression was inhibited by oxidative stress (reduced by 76.2%), hypoxia (reduced by 51.9%) and inflammatory factors (reduced by approximately 50%). These results suggested that the insufficient expression of PBK was involved in the poor endometrial thickness in TE.
conclusionsThe endometrial transcriptome in late-proliferative phase showed suppressed cell proliferation in women with thin endometria and decreased expression of PBK in human endometrial stromal cells (HESCs), to which inflammation and reactive oxygen species contributed.
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