ArticleReproduction (Cambridge, England)2019
CXCL16/CXCR6 interaction promotes endometrial decidualization via the PI3K/AKT pathway.
Article in Reproduction (Cambridge, England), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 90 citations in OpenAlex.
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- HBP1 enhances progesterone receptor activity and IGFBP1 expression driving endometrial decidualization.Communications biology · 2026Article
- Chemokines in Pregnancy.Biomolecules · 2025Review
- Altered Expression of CXCL16/CXCR6 and Its Correlation with Decidual Macrophage Polarization in Preeclampsia.International journal of women's health · 2025Article
- The role of CXCL16 in atherosclerosis: from mechanisms to therapy.Frontiers in immunology · 2025Review
- Exploration of the molecular characteristics and potential clinical significance of shared immune-related genes between preterm preeclampsia and term preeclampsia.BMC pregnancy and childbirth · 2024Article
- Can biomarkers identified from the uterine fluid transcriptome be used to establish a noninvasive endometrial receptivity prediction tool? A proof-of-concept study.Reproductive biology and endocrinology : RB&E · 2023Article
- An IGF1-expressing endometrial stromal cell population is associated with human decidualization.BMC biology · 2022Article
- Three categories of similarities between the placenta and cancer that can aid cancer treatment: Cells, the microenvironment, and metabolites.Frontiers in oncology · 2022Review
- Regulation and Function of Chemokines at the Maternal-Fetal Interface.Frontiers in cell and developmental biology · 2022Review
- Research on the Mechanism of Asperosaponin VI for Treating Recurrent Spontaneous Abortion by Bioinformatics Analysis and Experimental Validation.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Identification of 371 genetic variants for age at first sex and birth linked to externalising behaviour.Nature human behaviour · 2021Article
- Deciphering the Intercellular Communication Network of Peripartum Decidua that Orchestrates Delivery.Frontiers in cell and developmental biology · 2021Article
- Psychological Stress and Functional Endometrial Disorders: Update of Mechanism Insights.Frontiers in endocrinology · 2021Review
- Innate lymphoid cells are reduced in pregnant HIV positive women and are associated with preterm birth.Scientific reports · 2020Article
- The Transcriptome of Pig Spermatozoa, and Its Role in Fertility.International journal of molecular sciences · 2020Article
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Decidualization renders the endometrium transiently receptive to an implanting blastocyst although the underlying mechanisms remain incompletely understood. The aim of this study was to determine the role of chemokine CXCL16 and its receptor CXCR6 in the decidualization during pregnancy. Here, the expression of CXCL16 was investigated in endometrial tissues, decidua and placenta in this study. Compared with endometrial tissue, protein expression of CXCL16 was significantly higher in tissues from the fertile control samples, especially in villus. Meanwhile, the primary trophoblast cells and decidual stromal cells (DSCs) secreted more CXCL16 and expressed higher CXCR6 compared to endometrial stromal cells (ESCs) in vitro. Stimulation with the inducer of decidualization (8-bromoadenosine 3',5'-cyclic with medroxyprogesterone acetate, 8-Br-cAMP plus MPA) significantly upregulated the expression of CXCL16 and CXCR6 in ESCs in vitro. After treatment with exogenous recombinant human CXCL16 (rhCXCL16) or trophoblast-secreted CXLC16, decidualised ESCs showed a significant decidual response, mainly characterised by increased prolactin (PRL) secretion. Simultaneously, PI3K/PDK1/AKT/Cyclin D1 pathway in decidualised ESCs were activated by rhCXCL16, and AKT inhibitor GS 690693 abolished the PRL secretion of ESCs that was triggered by rhCXCL16. Finally, the impaired CXCL16/CXCR6 expression could be observed at the maternal-foetal interface from patients who have experienced spontaneous abortion. This study suggests that the CXCL16/CXCR6 axis contributes to the progression of ESC decidualization by activating PI3K/PDK1/AKT/Cyclin D1 pathway. It unveils a new paradigm at the maternal-foetal interface in which CXCL16 is an initiator for the molecular crosstalk that enhances decidualization of ESCs.
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