ReviewExperimental eye research2013
Smad3 is necessary for transforming growth factor-beta2 induced ocular hypertension in mice.
Review in Experimental eye research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
50 citing papers in PubMed, 78 citations in OpenAlex.
- Isobaric quantitative proteomics reveals altered extracellular matrix, cytoskeletal, and degradation pathways in glaucomatous trabecular meshwork cells.Scientific reports · 2026Article
- Pro-Homeostatic Effects of Estrogen on Intraocular Pressure and the Trabecular Meshwork.Investigative ophthalmology & visual science · 2026Article
- Article
- Regulation of toll-like receptor signaling pathways in age-related eye disease: from mechanisms to targeted therapeutics.Inflammopharmacology · 2025Review
- Single-cell profiling of trabecular meshwork identifies mitochondrial dysfunction in a glaucoma model that is protected by vitamin B3 treatment.bioRxiv : the preprint server for biology · 2025Article
- TGFβ2 alters segmental outflow and ECM ultrastructure in the trabecular meshwork.Experimental eye research · 2025Article
- Evaluation of Cross-Linked Actin Networks (CLANs) in Human Trabecular Meshwork Cells and Tissues.Methods in molecular biology (Clifton, N.J.) · 2025Article
- The Inducible TGFβ2 Ocular Hypertension Mouse Model.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Identification of Optic Nerve-Related Biomarkers in Primary Open-Angle Glaucoma Based on Comprehensive Bioinformatics and Mendelian Randomization.Translational vision science & technology · 2024Article
- GSK3β Inhibitors Inhibit TGFβ Signaling in the Human Trabecular Meshwork.Investigative ophthalmology & visual science · 2024Article
- Profiling IOP-Responsive Genes in the Trabecular Meshwork and Optic Nerve Head in a Rat Model of Controlled Elevation of Intraocular Pressure.Investigative ophthalmology & visual science · 2024Article
- Development and Verification of a Novel Three-Dimensional Aqueous Outflow Model for High-Throughput Drug Screening.Bioengineering (Basel, Switzerland) · 2024Article
- Molecular pathways in experimental glaucoma models.Frontiers in neuroscience · 2024Review
- Inhibition of TGF-β2-Induced Trabecular Meshwork Fibrosis by Pirfenidone.Translational vision science & technology · 2023Article
- Aqueous Humor TGF-β2 and Its Association With Intraocular Pressure in a Naturally Occurring Large Animal Model of Glaucoma.Investigative ophthalmology & visual science · 2023Article
- A method describing the microdissection of trabecular meshwork tissue from Brown Norway rat eyes.Experimental eye research · 2023Article
- Microbiome Dysbiosis: A Pathological Mechanism at the Intersection of Obesity and Glaucoma.International journal of molecular sciences · 2023Review
- Mechanism of action of non-coding RNAs and traditional Chinese medicine in myocardial fibrosis: Focus on the TGF-β/Smad signaling pathway.Frontiers in pharmacology · 2023Review
- Viral Vector-Induced Ocular Hypertension in Mice.Methods in molecular biology (Clifton, N.J.) · 2023Article
- CCN2/CTGF tip the balance of growth factors towards TGF-β2 in primary open-angle glaucoma.Frontiers in molecular biosciences · 2023Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
TGFβ2 induces extracellular matrix (ECM) remodeling and alters the cytoskeleton by both the canonical Smad and non-canonical signaling pathways. TGFβ2 regulates the expression of ECM proteins in trabecular meshwork (TM) cells, increases intraocular pressure (IOP) in an ex vivo perfusion organ culture model, and induces ocular hypertension in rodent eyes. A necessary step in the canonical Smad signaling pathway is phosphorylation of receptor protein Smad3 by the TGF-β receptor complex. The purpose of this study was to determine whether TGFβ2 signals in vivo through the canonical Smad signaling pathway in the TM using Smad3 knockout (KO) mice. Ad5.hTGFβ2(226/228) (2.5 × 10(7) pfu) was injected intravitreally into one eye of homozygous (WT), heterozygous (HET), and homozygous (KO) 129-Smad3(tm1Par)/J mice (n = 9-10 mice/group), with the uninjected contralateral eye serving as the control. IOP measurements were taken using a rebound tonometer. To test the effect of TGFβ2 signaling on the ECM, fibronectin expression was determined by immunohistochemistry and qPCR analysis. Transduction of the TM with viral vector Ad5.hTGFβ2(226/228) caused a statistically significant difference in IOP exposure between Smad3 genotypes: WT, 187.7 ± 23.9 mmHg*day (n = 9); HET, 95.6 ± 24.5 mmHg*day (n = 9); KO, 52.8 ± 25.2 mmHg*day (n = 10); (p < 0.05 WT versus HET, p < 0.01 WT versus KO). Immunohistochemistry and qPCR analysis showed that Ad5.hTGFβ2(226/228) increased fibronectin expression in the TM of WT mice (2.23 ± 0.24 fold) compared to Smad3 KO mice (0.99 ± 0.19 fold), p < 0.05. These results demonstrate Smad3 is a necessary signaling protein for TGFβ2-induced ocular hypertension and fibronectin deposition in the TM.
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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.