Evidence map›Paper›PMID 42786592›Full record

ArticleStem cells (Dayton, Ohio)2026

EPLIN stabilizes cell-cell adhesion complexes to facilitate TGF-β1-induced fibroblastic differentiation of human periodontal ligament stem cells.

A-Hyeong Choi, Seon-Yle Ko, Young-Joo Jang

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Article in Stem cells (Dayton, Ohio), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

3 authors.

A-Hyeong ChoiDepartment of Manobiomedical Science & BK21 FOUR NBM Global Research Center for Regenerative Medicine, Dankook University, Cheonan 31116, Korea.
Seon-Yle KoDepartment of Oral Biochemistry, School of Dentistry, Dankook University, Cheonan 31116, Korea.
Young-Joo JangDepartment of Manobiomedical Science & BK21 FOUR NBM Global Research Center for Regenerative Medicine, Dankook University, Cheonan 31116, Korea.ORCID 0000-0001-5200-7341

Funding

Medical Research Center RS-2021-NR060095Mid-Career Researcher RS-2025-19612991
6 · The paper itself

Abstract

objectivesPeriodontal ligament stem cells (hPDLSCs) are essential for periodontal regeneration, yet the molecular mechanisms governing their differentiation into functional fibroblasts remain poorly understood. This study aimed to identify novel regulatory molecules of PDL fibroblastic differentiation and elucidate the role of epithelial protein lost in neoplasm (EPLIN) in the fibroblastic differentiation.

methodshPDLSCs were differentiated into PDL fibroblasts using TGF-β1. A novel antibody (anti-LG45) identified EPLIN as a target antigen. Functional roles of EPLIN were investigated through siRNA-mediated depletion and ectopic overexpression. Phalloidin staining for F-actin and co-immunoprecipitation were performed to analyze adherens junction integrity.

resultsTGF-β1 treatment successfully induced fibroblastic differentiation, as evidenced by significant increases in fibroblastic marker expressions, which were abolished by the TGF-β receptor inhibitor SB-431542. A novel anti-LG45 antibody was found to specifically recognize EPLIN in differentiated PDL fibroblasts. EPLIN depletion significantly reduced the fibroblastic differentiation and disrupted the typical elongated morphology of PDL fibroblasts. Mechanistically, EPLIN depletion led to filament fragmentation and cytoskeletal collapse, decoupled N-cadherin from the cytoskeleton, and accelerated cell proliferation. Conversely, ectopic overexpression of EPLIN-α or β was sufficient to inhibit proliferation and induce fibroblastic markers even without TGF-β1 stimulation.

conclusionEPLIN is a key regulatory factor that stabilizes the linkage between the actin cytoskeleton and adherens junctions, maintaining the fibroblastic phenotype and preventing unscheduled proliferation in hPDLSCs. This study indicates the importance of cytoskeletal structural integrity in PDL differentiation. Under this circumstance, EPLIN serves as a regulator that maintains the fibroblastic differentiation state of hPDLSCs and prevents unscheduled proliferation.

Indexed as

Cell DifferentiationCytoskeletal ProteinsFibroblastsPeriodontal LigamentStem CellsTransforming Growth Factor beta1Cell AdhesionCells, CulturedHumansCytoskeletal ProteinsTransforming Growth Factor beta1adherens junctionepithelial protein lost in neoplasm (EPLIN)human periodontal ligament stem cells (hPDLSCs)PDL fibroblastic differentiationTGF-β1

Identifiers

PMID42786592
PMCPMC13653676

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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.