ArticleThe Journal of biological chemistry2012
Epithelial protein lost in neoplasm (EPLIN) interacts with α-catenin and actin filaments in endothelial cells and stabilizes vascular capillary network in vitro.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 75 citations in OpenAlex.
- EPLIN stabilizes cell-cell adhesion complexes to facilitate TGF-β1-induced fibroblastic differentiation of human periodontal ligament stem cells.Stem cells (Dayton, Ohio) · 2026Article
- A specific role for endothelial EPLIN-isoform-regulated actin dynamics in neutrophil transmigration.Scientific reports · 2025Article
- Ubiquitination of VE-cadherin regulates inflammation-induced vascular permeability in vivo.EMBO reports · 2024Article
- The concerted action of SEPT9 and EPLIN modulates the adhesion and migration of human fibroblasts.Life science alliance · 2024Article
- Lipotoxic hepatocyte derived LIMA1 enriched small extracellular vesicles promote hepatic stellate cells activation via inhibiting mitophagy.Cellular & molecular biology letters · 2024Article
- Exploring the Enigma: The Role of the Epithelial Protein Lost in Neoplasm in Normal Physiology and Cancer Pathogenesis.International journal of molecular sciences · 2024Review
- Characterization of LIMA1 and its emerging roles and potential therapeutic prospects in cancers.Frontiers in oncology · 2023Review
- EPLINβ Is Involved in the Assembly of Cadherin-catenin Complexes in Osteoblasts and Affects Bone Formation.Acta histochemica et cytochemica · 2022Article
- Lima1 mediates the pluripotency control of membrane dynamics and cellular metabolism.Nature communications · 2022Article
- Epithelial Protein Lost in Neoplasm, EPLIN, the Cellular and Molecular Prospects in Cancers.Biomolecules · 2021Review
- A junctional PACSIN2/EHD4/MICAL-L1 complex coordinates VE-cadherin trafficking for endothelial migration and angiogenesis.Nature communications · 2021Article
- Article
- Epithelial protein lost in neoplasm (EPLIN) and prostate cancer: lessons learned from the ARCaP model.American journal of clinical and experimental urology · 2021Review
- Autoregulatory "Multitasking" at Endothelial Cell Junctions by Junction-Associated Intermittent Lamellipodia Controls Barrier Properties.Frontiers in physiology · 2020Review
- Vascular Endothelial (VE)-Cadherin, Endothelial Adherens Junctions, and Vascular Disease.Cold Spring Harbor perspectives in biology · 2018Review
- Equine skeletal muscle adaptations to exercise and training: evidence of differential regulation of autophagosomal and mitochondrial components.BMC genomics · 2017Article
- Vinculin in cell-cell and cell-matrix adhesions.Cellular and molecular life sciences : CMLS · 2017Review
- Epithelial protein lost in neoplasm (EPLIN): Beyond a tumor suppressor.Genes & diseases · 2017Review
- Discovery of a ROCK inhibitor, FPND, which prevents cerebral hemorrhage through maintaining vascular integrity by interference with VE-cadherin.Cell death discovery · 2017Article
- Cell-cell junctional mechanotransduction in endothelial remodeling.Cellular and molecular life sciences : CMLS · 2017Review
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
Adherens junctions are required for vascular endothelium integrity. These structures are formed by the clustering of the homophilic adhesive protein VE-cadherin, which recruits intracellular partners, such as β- and α-catenins, vinculin, and actin filaments. The dogma according to which α-catenin bridges cadherin·β-catenin complexes to the actin cytoskeleton has been challenged during the past few years, and the link between the VE-cadherin·catenin complex and the actin cytoskeleton remains unclear. Recently, epithelial protein lost in neoplasm (EPLIN) has been proposed as a possible bond between the E-cadherin·catenin complex and actin in epithelial cells. Herein, we show that EPLIN is expressed at similar levels in endothelial and epithelial cells and is located at interendothelial junctions in confluent cells. Co-immunoprecipitation and GST pulldown experiments provided evidence that EPLIN interacts directly with α-catenin and tethers the VE-cadherin·catenin complex to the actin cytoskeleton. In the absence of EPLIN, vinculin was delocalized from the junctions. Furthermore, suppression of actomyosin tension using blebbistatin triggered a similar vinculin delocalization from the junctions. In a Matrigel assay, EPLIN-depleted endothelial cells exhibited a reduced capacity to form pseudocapillary networks because of numerous breakage events. In conclusion, we propose a model in which EPLIN establishes a link between the cadherin·catenin complex and actin that is independent of actomyosin tension. This link acts as a mechanotransmitter, allowing vinculin binding to α-catenin and formation of a secondary molecular bond between the adherens complex and the cytoskeleton through vinculin. In addition, we provide evidence that the EPLIN clutch is necessary for stabilization of capillary structures in an angiogenesis model.
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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.