ArticleReproductive sciences (Thousand Oaks, Calif.)2010
Basal and steroid hormone-regulated expression of CXCR4 in human endometrium and endometriosis.
Article in Reproductive sciences (Thousand Oaks, Calif.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 51 citations in OpenAlex.
- Anti-Angiogenic RNAi-Based Treatment of Endometriosis in a Rat Model Using CXCR4-Targeted Peptide Nanoparticles.International journal of molecular sciences · 2025Article
- Different Effect of Dienogest on Endometrium Mesenchymal Stem Cells Derived from Healthy and Endometriosis TissuesBalkan medical journal · 2024Article
- Dissecting theBiomedicines · 2022Article
- Loss of Cxcr4 in Endometriosis Reduces Proliferation and Lesion Number while Increasing Intraepithelial Lymphocyte Infiltration.The American journal of pathology · 2021Article
- Anti-angiogenic treatment of endometriosis via anti-VEGFA siRNA delivery by means of peptide-based carrier in a rat subcutaneous model.Gene therapy · 2018Article
- Effects of histone methyltransferase inhibition in endometriosis.Biology of reproduction · 2018Article
- G-Protein-Coupled Receptor CXCR7 Is Overexpressed in Human and Murine Endometriosis.Reproductive sciences (Thousand Oaks, Calif.) · 2018Article
- Pharmacological blockage of the CXCR4-CXCL12 axis in endometriosis leads to contrasting effects in proliferation, migration, and invasion.Biology of reproduction · 2018Article
- Bone Marrow Stem Cell Chemotactic Activity Is Induced by Elevated CXCl12 in Endometriosis.Reproductive sciences (Thousand Oaks, Calif.) · 2017Article
- MicroRNA expression profiles and networks in CXCL12‑stimulated human endometrial stromal cells.Molecular medicine reports · 2017Article
- Autophagy in endometriosis.American journal of translational research · 2017Review
- Endometriosis: where are we and where are we going?Reproduction (Cambridge, England) · 2016Review
- The Role of Stem Cells in the Etiology and Pathophysiology of Endometriosis.Seminars in reproductive medicine · 2015Review
- Pathogenesis of Endometriosis: Roles of Retinoids and Inflammatory Pathways.Seminars in reproductive medicine · 2015Review
- Chemoattraction of bone marrow-derived stem cells towards human endometrial stromal cells is mediated by estradiol regulated CXCL12 and CXCR4 expression.Stem cell research · 2015Article
- Survival outcomes in endometrial cancer patients are associated with CXCL12 and estrogen receptor expression.International journal of cancer · 2012Article
- HDAC1 and HDAC2 are differentially expressed in endometriosis.Reproductive sciences (Thousand Oaks, Calif.) · 2012Article
- Endometriosis: hormone regulation and clinical consequences of chemotaxis and apoptosis.Human reproduction updateReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Endometriosis is associated with activation of local and systemic inflammatory mechanisms, including increased levels of chemokines and other proinflammatory cytokines. We have previously reported increased gene expression of chemokine receptor 4 (CXCR4), the receptor for CXCL12, in lesions of the rat model of endometriosis. The CXCR4-CXCL12 axis has been shown to have both immune (HIV infection, lymphocyte chemotaxis) and nonimmune functions, including roles in tissue repair, angiogenesis, invasion, and migration. There is evidence indicating that these mechanisms are also at play in endometriosis; therefore, we hypothesized that activation of the CXCR4-CXCL12 axis could be responsible, at least in part, for the survival and establishment of endometrial cells ectopically. Immunohistochemistry (IHC) showed that CXCR4 protein levels were significantly higher in endometriotic lesions compared to the endometrium of controls. Next, we determined basal gene and protein expression of CXCR4 and CXCL12 and regulation by estradiol (E2) and/or progesterone (P4) in endometrial cell lines using quantitative polymerase chain reaction (qPCR), and Western blots. Basal CXCR4 gene expression levels were higher in epithelial versus stromal cells; conversely, CXCL12 was expressed at higher levels in stromal vs epithelial cells. CXCR4 gene expression was significantly downregulated by ovarian steroid hormones in endometrial epithelial. These data suggest that steroid modulation of CXCR4 is defective in endometriosis, although the specific mechanism involved remains to be elucidated. These findings have implications for future therapeutic strategies specifically targeting the inflammatory component in endometriosis.
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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.