ArticleMolecular vision2012
Smad7 siRNA inhibit expression of extracellular matrix in trabecular meshwork cells treated with TGF-β2.
Article in Molecular vision, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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
9 citing papers in PubMed, 16 citations in OpenAlex.
- TGFβ2 alters segmental outflow and ECM ultrastructure in the trabecular meshwork.Experimental eye research · 2025Article
- Glaucoma: Novel antifibrotic therapeutics for the trabecular meshwork.European journal of pharmacology · 2023Review
- Genome-wide transcriptome profiling of human trabecular meshwork cells treated with TGF-β2.Scientific reports · 2022Article
- miR-486-5p Restrains Extracellular Matrix Production and Oxidative Damage in Human Trabecular Meshwork Cells by Targeting TGF-Journal of ophthalmology · 2022Article
- Non-Pigmented Ciliary Epithelium-Derived Extracellular Vesicles Loaded with SMAD7 siRNA Attenuate Wnt Signaling in Trabecular Meshwork Cells In Vitro.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Computational analysis for identification of the extracellular matrix molecules involved in endometrial cancer progression.PloS one · 2020Article
- miR-590 promotes the proliferation of HUMSCs and induces ECM synthesis by targeting Smad7.Oncology letters · 2017Article
- Adenovirus conducted connective tissue growth factor on extracellular matrix in trabecular meshwork and its role on aqueous humor outflow facility.Molecular biology reports · 2013Article
- Small-interfering RNAs (siRNAs) as a promising tool for ocular therapy.British journal of pharmacology · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeExtracellular matrix (ECM) deposits lead to elevated resistance of aqueous humor outflow which play an important role in the development of primary open angle glaucoma (POAG). The TGF-β2 (transforming growth factor β)/Smad (signaling mathers against decapentaplegic) pathway is known to regulate the ECM deposits. In this study, we determined the effect of Smad7 siRNA transfection in inhibiting the expression of ECM components.
methodsPlasmid containing Smad7 siRNA was used to transfect cultured human trabecular meshwork cells (HTM). Protein expression of Smad7, fibronectin, and laminin was determined using western blot.
resultsDownregulation of Smad7 interrupts the effects of TGF-β2 on the expression of several ECM components. Smad7 siRNA can partially decrease the expression of Smad7, fibronectin, and laminin.
conclusionsSmad7 plays an important role in regulating the ECM protein in the aqueous outflow pathway.
Indexed as
Identifiers
22876112PMC3413437W2133401139What OpenQuestion holds
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.