ArticleInvestigative ophthalmology & visual science2017
TGFβ2 Induces the Formation of Cross-Linked Actin Networks (CLANs) in Human Trabecular Meshwork Cells Through the Smad and Non-Smad Dependent Pathways.
Article in Investigative ophthalmology & visual science, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 75 citations in OpenAlex.
- Modeling of Lowe Patient-Derived Induced Pluripotent Stem Cells Into Trabecular Meshwork.American journal of ophthalmology · 2026Article
- Cross-linked actin networks (CLANs) and their role in the trabecular meshwork.Experimental eye research · 2026Review
- Effect of Rho Kinase Inhibitor RKI-1447 on Dexamethasone-Induced Ocular Hypertension and Its Molecular Mechanisms in Sprague-Dawley Rats.Drug design, development and therapy · 2026Article
- TGF-β: elusive target in diabetic kidney disease.Renal failure · 2025Review
- TRPV4 activation by TGFβ2 enhances cellular contractility and drives ocular hypertension.eLife · 2025Article
- TGFβ2 alters segmental outflow and ECM ultrastructure in the trabecular meshwork.Experimental eye research · 2025Article
- Fibrosis-Related Gene and Protein Expression in Normal and Glaucomatous Trabecular Meshwork Cells.Investigative ophthalmology & visual science · 2025Article
- Characterization, Enrichment, and Computational Modeling of Cross-Linked Actin Networks in Transformed Trabecular Meshwork Cells.Investigative ophthalmology & visual science · 2025Article
- Evaluation of Cross-Linked Actin Networks (CLANs) in Human Trabecular Meshwork Cells and Tissues.Methods in molecular biology (Clifton, N.J.) · 2025Article
- The role of YAP/TAZ mechanosignaling in trabecular meshwork and Schlemm's canal cell dysfunction.Vision research · 2024Review
- Congenital microcoria deletion in mouse links Sox21 dysregulation to disease and suggests a role for TGFB2 in glaucoma and myopia.American journal of human genetics · 2024Article
- Characterization, enrichment, and computational modeling of cross-linked actin networks in trabecular meshwork cells.bioRxiv : the preprint server for biology · 2024Article
- GSK3β Inhibitors Inhibit TGFβ Signaling in the Human Trabecular Meshwork.Investigative ophthalmology & visual science · 2024Article
- Proteomics Analyses of Small Extracellular Vesicles of Aqueous Humor: Identification and Validation of GAS6 and SPP1 as Glaucoma Markers.International journal of molecular sciences · 2024Article
- Glucocorticoid-Induced Ocular Hypertension and Glaucoma.Clinical ophthalmology (Auckland, N.Z.) · 2024Review
- Therapeutic applications of CRISPR/Cas9 gene editing technology for the treatment of ocular diseases.The FEBS journal · 2023Review
- Aqueous Humor TGF-β2 and Its Association With Intraocular Pressure in a Naturally Occurring Large Animal Model of Glaucoma.Investigative ophthalmology & visual science · 2023Article
- High VEGF Concentrations Accelerate Human Trabecular Meshwork Fibrosis in a TAZ-Dependent Manner.International journal of molecular sciences · 2023Article
- Microbiome Dysbiosis: A Pathological Mechanism at the Intersection of Obesity and Glaucoma.International journal of molecular sciences · 2023Review
- YAP/TAZ Mediate TGFβ2-Induced Schlemm's Canal Cell Dysfunction.Investigative ophthalmology & visual science · 2022Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Purpose: Increased intraocular pressure results from increased aqueous humor (AH) outflow resistance at the trabecular meshwork (TM) due to pathologic changes including the formation of cross-linked actin networks (CLANs). Transforming growth factor β2 (TGFβ2) is elevated in the AH and TM of primary open angle glaucoma (POAG) patients and induces POAG-associated TM changes, including CLANs. We determined the role of individual TGFβ2 signaling pathways in CLAN formation. Methods: Cultured nonglaucomatous human TM (NTM) cells were treated with control or TGFβ2, with or without the inhibitors of TGFβ receptor, Smad3, c-Jun N-terminal kinases (JNK), extracellular signal regulated kinase (ERK), P38, or Rho-associated protein kinase (ROCK). NTM cells were cotreated with TGFβ2 plus inhibitors for 10 days or pretreated with TGFβ2 for 10 days followed by 1-hour inhibitor treatment. NTM cells were immunostained with phalloidin-Alexa-488 and 4',6-diamidino-2-phenylindole (DAPI). Data were analyzed using 1-way ANOVA and Dunnett's post hoc test. Results: TGFβ2 significantly induced CLAN formation (n = 6 to 12, P < 0.05), which was completely inhibited by TGFβ receptor, Smad3, and ERK inhibitors, as well as completely or partially inhibited by JNK, P38, and ROCK inhibitors, depending on cell strains. One-hour exposure to ROCK inhibitor completely resolved formed CLANs (P < 0.05), whereas TGFβ receptor, Smad3 inhibitor, and ERK inhibitors resulted in partial or complete resolution. The JNK and P38 inhibitors showed partial or no resolution. Among these inhibitors, the ROCK inhibitor was the most disruptive to the actin stress fibers, whereas ERK inhibition showed the least disruption. Conclusions: TGFβ2-induced CLANs in NTM cells were prevented and resolved using various pathway inhibitors. Apart from CLAN inhibition, some of these inhibitors also had different effects on actin stress fibers.
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