ArticlePloS one2015
Aquaporin 5 Plays a Role in Estrogen-Induced Ectopic Implantation of Endometrial Stromal Cells in Endometriosis.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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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.
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Who cites it
17 citing papers in PubMed, 32 citations in OpenAlex.
- Migratory responses in enucleated cells: The forces driving the locomotion movement of unicellular organisms.PNAS nexus · 2025Article
- AutoDock and molecular dynamics-based therapeutic potential prediction of flavonoids for primary Sjögren's syndrome.Heliyon · 2024Article
- Aquaporins: Potential Targets in Inflammatory Diseases.The Eurasian journal of medicine · 2023Article
- Aquaporin-mediated dysregulation of cell migration in disease states.Cellular and molecular life sciences : CMLS · 2023Review
- Aquaporin-5 Dynamic Regulation.International journal of molecular sciences · 2023Review
- Methods for studying mammalian aquaporin biology.Biology methods & protocols · 2023Review
- Signaling Mechanisms and Pharmacological Modulators Governing Diverse Aquaporin Functions in Human Health and Disease.International journal of molecular sciences · 2022Review
- Apigenin, a Single Active Component of Herbal Extract, Alleviates XerostomiaFrontiers in pharmacology · 2022Article
- Article
- Targeting Aquaporins in Novel Therapies for Male and Female Breast and Reproductive Cancers.Cells · 2021Review
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- Differential expression and inhibitory effects of aquaporins on the development of adenomyosis.Molecular medicine reports · 2020Article
- Article
- Ion Channels in The Pathogenesis of Endometriosis: A Cutting-Edge Point of View.International journal of molecular sciences · 2020Review
- Aquaporin-3 mediates ovarian steroid hormone-induced motility of endometrial epithelial cells.Human reproduction (Oxford, England) · 2018Article
- Estrogen nuclear receptors affect cell migration by altering sublocalization of AQP2 in glioma cell lines.Cell death discovery · 2018Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aquaporin 5 (AQP5) participates in the migration of endometrial cells. Elucidation of the molecular mechanisms associated with AQP5-mediated, migration of endometrial cells may contribute to a better understanding of endometriosis. Our objectives included identifying the estrogen-response element (ERE) in the promoter region of the AQP5 gene, and, investigating the effects of AQP5 on ectopic implantation of endometrial cells. Luciferase reporter assays and electrophoretic mobility shift assay (EMSA) identified the ERE-like motif in the promoter region of the AQP5 gene. After blocking and up-regulating estradiol (E2) levels, we analysed the expression of AQP5 in endometrial stromal (ES) cells. After blocking E2 /or phosphatidylinositol 3 kinase(PI3K), we analysed the role of AQP5 in signaling pathways. We constructed an AQP5, shRNA, lentiviral vector to knock out the AQP5 gene in ES cells. After knock-out of the AQP5 gene, we studied the role of AQP5 in cell invasion, proliferation, and the formation of ectopic endometrial implants in female mice. We identified an estrogen-response element in the promoter region of the AQP5 gene. Estradiol (E2) increased AQP5 expression in a dose-dependent fashion, that was blocked by ICI182,780(an estrogen receptor inhibitor). E2 activated PI3K /protein kinase B(AKT) pathway (PI3K/AKT), that, in turn, increased AQP5 expression. LY294002(PI3K inhibitor) attenuated estrogen-enhanced, AQP5 expression. Knock-out of the AQP5 gene with AQP5 shRNA lentiviral vector significantly inhibited E2-enhanced invasion, proliferation of ES cells and formation of ectopic implants. Estrogen induces AQP5 expression by activating ERE in the promoter region of the AQP5gene, activates the PI3K/AKT pathway, and, promotes endometrial cell invasion and proliferation. These results provide new insights into some of the mechanisms that may underpin the development of deposits of ectopic endometrium.
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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.