ArticleThe Prostate2019
E-cadherin is downregulated in benign prostatic hyperplasia and required for tight junction formation and permeability barrier in the prostatic epithelial cell monolayer.
Article in The Prostate, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 27 citations in OpenAlex.
- Lipid and Foam Cell Accumulation as Novel Pathological Features of Benign Prostatic Hyperplasia.The Prostate · 2026Article
- Comprehensive biochemical insights into derivatives of PSA and glycosylation-specific changes in PSA: role in diagnosis and management of prostate cancer.Clinical proteomics · 2026Review
- Prostate Tissue-Induced Platelet Activation and Platelet-Neutrophil Aggregation Following Transurethral Resection of the Prostate Surgery: An In Vitro Study.Biomedicines · 2025Article
- Effects of small extracellular vesicles derived from normoxia- and hypoxia-treated prostate cancer cells on the submandibular salivary gland epitheliumTissue barriers · 2025Article
- The Blood-prostate Barrier: An Obstacle to Drug Delivery into the Prostate.Current drug delivery · 2025Review
- Article
- Effects of oral administration of nonselective Trk inhibitor on bladder overactivity in rodent models of prostatic inflammation.The Prostate · 2024Article
- A Detailed Clinical Case of Localized Prostate Tumors Treated with Nanoparticle-Assisted Sub-Ablative Laser Ablation.Nanomaterials (Basel, Switzerland) · 2024Article
- Intrinsic and extrinsic factors causing hyperplasia of the prostate.International journal of urology : official journal of the Japanese Urological Association · 2024Review
- The Multifaceted Role of Osteopontin in Prostate Pathologies.Biomedicines · 2023Review
- Simvastatin Improves Benign Prostatic Hyperplasia: Role of Peroxisome-Proliferator-Activated Receptor-γ and Classic WNT/β-Catenin Pathway.International journal of molecular sciences · 2023Article
- The Emerging Role of Cell Adhesion Molecules on Benign Prostatic Hyperplasia.International journal of molecular sciences · 2023Review
- Article
- Changes in the Expression and Functional Activities of C-X-C Motif Chemokine Ligand 13 (International journal of molecular sciences · 2022Article
- Article
- E-cadherin deficiency promotes prostate macrophage inflammation and bladder overactivity in aged male mice.Aging · 2022Article
- Applications of Vertebrate Models in Studying Prostatitis and Inflammation-Associated Prostatic Diseases.Frontiers in molecular biosciences · 2022Review
- E-cadherin expression is inversely correlated with aging and inflammation in the prostate.American journal of clinical and experimental urology · 2021Article
- Claudin-1 down-regulation in the prostate is associated with aging and increased infiltration of inflammatory cells in BPH.American journal of clinical and experimental urology · 2021Article
- Prostate-Specific Deletion of Cdh1 Induces Murine Prostatic Inflammation and Bladder Overactivity.Endocrinology · 2021Article
Corrections and comments
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Authors and funding
24 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundWe previously reported the presence of prostate-specific antigen (PSA) in the stromal compartment of benign prostatic hyperplasia (BPH). Since PSA is expressed exclusively by prostatic luminal epithelial cells, PSA in the BPH stroma suggests increased tissue permeability and the compromise of epithelial barrier integrity. E-cadherin, an important adherens junction component and tight junction regulator, is known to exhibit downregulation in BPH. These observations suggest that the prostate epithelial barrier is disrupted in BPH and E-cadherin downregulation may increase epithelial barrier permeability.
methodsThe ultra-structure of cellular junctions in BPH specimens was observed using transmission electron microscopy (TEM) and E-cadherin immunostaining analysis was performed on BPH and normal adjacent specimens from BPH patients. In vitro cell line studies using benign prostatic epithelial cell lines were performed to determine the impact of small interfering RNA knockdown of E-cadherin on transepithelial electrical resistance and diffusion of fluorescein isothiocyanate (FITC)-dextran in transwell assays.
resultsThe number of kiss points in tight junctions was reduced in BPH epithelial cells as compared with the normal adjacent prostate. Immunostaining confirmed E-cadherin downregulation and revealed a discontinuous E-cadherin staining pattern in BPH specimens. E-cadherin knockdown increased monolayer permeability and disrupted tight junction formation without affecting cell density.
conclusionsOur results indicate that tight junctions are compromised in BPH and loss of E-cadherin is potentially an important underlying mechanism, suggesting targeting E-cadherin loss could be a potential approach to prevent or treat BPH.
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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.