ArticleScientific reports2020
Glucocorticoid-induced cell-derived matrix modulates transforming growth factor β2 signaling in human trabecular meshwork cells.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- Natural and iatrogenic ocular manifestations of rheumatoid arthritis: a systematic review.International ophthalmology · 2022Pooled it
- Chromatin dynamics identifies 78 genes at loci associated with elevated intraocular pressure and primary open-angle glaucoma.bioRxiv : the preprint server for biology · 2026Article
- Pro-Homeostatic Effects of Estrogen on Intraocular Pressure and the Trabecular Meshwork.Investigative ophthalmology & visual science · 2026Article
- Divergence in cellular markers observed in single-cell transcriptomics datasets between cultured primary trabecular meshwork cells and tissues.Scientific data · 2025Article
- Influence of dexamethasone-induced matrices on the TM transcriptome.Experimental eye research · 2024Article
- To be or not to be - Decoding the Trabecular Meshwork Cell Identity.bioRxiv : the preprint server for biology · 2024Article
- ECM biomaterials for modeling of outflow cell biology in health and disease.Biomaterials and biosystems · 2024Article
- Article
- Characterization of extracellular matrix deposited by segmental trabecular meshwork cells.bioRxiv : the preprint server for biology · 2023Article
- TGF-β-3 Induces Different Effects from TGF-β-1 and -2 on Cellular Metabolism and the Spatial Properties of the Human Trabecular Meshwork Cells.International journal of molecular sciences · 2023Article
- Human Trabecular Meshwork (HTM) Cells Treated with TGF-β2 or Dexamethasone Respond to Compression Stress in Different Manners.Biomedicines · 2022Article
- Short and long-term effect of dexamethasone on the transcriptome profile of primary human trabecular meshwork cells in vitro.Scientific reports · 2022Article
- Endogenous expression of Notch pathway molecules in human trabecular meshwork cells.Experimental eye research · 2022Article
- Impact of systemic steroids combined with immunosuppressive treatment on glaucomatous features in patients with systemic lupus erythematosus.International journal of ophthalmology · 2022Article
- The role of Vitamin D3 in ocular fibrosis and its therapeutic potential for the glaucomatous trabecular meshwork.Frontiers in ophthalmology · 2022Review
- Autotaxin May Have Lysophosphatidic Acid-Unrelated Effects on Three-Dimension (3D) Cultured Human Trabecular Meshwork (HTM) Cells.International journal of molecular sciences · 2021Article
- Establishment of appropriate glaucoma models using dexamethasone or TGFβ2 treated three-dimension (3D) cultured human trabecular meshwork (HTM) cells.Scientific reports · 2021Article
- mTOR inhibitors potentially reduce TGF-β2-induced fibrogenic changes in trabecular meshwork cells.Scientific reports · 2021Article
- Long non-coding RNA HULC regulates TLR4 expression by acting as ceRNA to attract miR-663b in skin fibroblasts of pediatric burns.American journal of translational research · 2021Article
- Lysophosphatidic Acid and IL-6 Trans-signaling Interact via YAP/TAZ and STAT3 Signaling Pathways in Human Trabecular Meshwork Cells.Investigative ophthalmology & visual science · 2020Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Aberrant remodeling of trabecular meshwork (TM) extracellular matrix (ECM) may induce ocular hypertensive phenotypes in human TM (hTM) cells to cause ocular hypertension, via a yet unknown mechanism. Here, we show that, in the absence of exogenous transforming growth factor-beta2 (TGFβ2), compared with control matrices (VehMs), glucocorticoid-induced cell-derived matrices (GIMs) trigger non-Smad TGFβ2 signaling in hTM cells, correlated with overexpression/activity of structural ECM genes (fibronectin, collagen IV, collagen VI, myocilin), matricellular genes (connective tissue growth factor [CTGF], secreted protein, acidic and rich in cysteine), crosslinking genes/enzymes (lysyl oxidase, lysyl oxidase-like 2-4, tissue transglutaminase-2), and ECM turnover genes/enzymes (matrix metalloproteinases-MMP2,14 and their inhibitors-TIMP2). However, in the presence of exogenous TGFβ2, VehMs and GIMs activate Smad and non-Smad TGFβ2 signaling in hTM cells, associated with overexpression of α-smooth muscle actin (α-SMA), and differential upregulation of aforementioned ECM genes/proteins with new ones emerging (collagen-I, thrombospondin-I, plasminogen activator inhibitor, MMP1, 9, ADAMTS4, TIMP1); with GIM-TGFβ2-induced changes being mostly more pronounced. This suggests dual glaucomatous insults potentiate profibrotic signaling/phenotypes. Lastly, we demonstrate type I TGFβ receptor kinase inhibition abrogates VehM-/GIM- and/or TGFβ2-induced upregulation of α-SMA and CTGF. Collectively, pathological TM microenvironments are sufficient to elicit adverse cellular responses that may be ameliorated by targeting TGFβ2 pathway.
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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 Socratic graph.