ArticlePloS one2012
Troglitazone attenuates TGF-β1-induced EMT in alveolar epithelial cells via a PPARγ-independent mechanism.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 31 citations in OpenAlex.
- The interplay of ferroptosis and oxidative stress in pulmonary fibrosis: from mechanisms to treatment.Frontiers in cell and developmental biology · 2026Review
- Advancing therapeutic frontiers: a pipeline of novel drugs for luminal and perianal Crohn's disease management.Therapeutic advances in gastroenterology · 2024Review
- Potential therapeutic effects of peroxisome proliferator-activated receptors on corneal diseases.Experimental biology and medicine (Maywood, N.J.) · 2024Review
- Article
- Cellular mechanotransduction in health and diseases: from molecular mechanism to therapeutic targets.Signal transduction and targeted therapy · 2023Review
- Alveolar type 2 epithelial cell senescence and radiation-induced pulmonary fibrosis.Frontiers in cell and developmental biology · 2022Review
- Article
- PPARγ agonists: potential treatment for autism spectrum disorder by inhibiting the canonical WNT/β-catenin pathway.Molecular psychiatry · 2019Review
- Warburg effect hypothesis in autism Spectrum disorders.Molecular brain · 2018Review
- Hyperoxia induces paracellular leak and alters claudin expression by neonatal alveolar epithelial cells.Pediatric pulmonology · 2018Article
- Thermodynamic Aspects and Reprogramming Cellular Energy Metabolism during the Fibrosis Process.International journal of molecular sciences · 2017Review
- Trichostatin A inhibits radiation-induced epithelial-to-mesenchymal transition in the alveolar epithelial cells.Oncotarget · 2017Article
- Thalidomide Inhibits TGF-β1-induced Epithelial to Mesenchymal Transition in Alveolar Epithelial Cells via Smad-Dependent and Smad-Independent Signaling Pathways.Scientific reports · 2017Article
- Runx3 is a key modulator during the epithelial-mesenchymal transition of alveolar type II cells in animal models of BPD.International journal of molecular medicine · 2017Article
- Interactions between TGF-β1, canonical WNT/β-catenin pathway and PPAR γ in radiation-induced fibrosis.Oncotarget · 2017Review
- Anti-fibrogenic effect of PPAR-γ agonists in human intestinal myofibroblasts.BMC gastroenterology · 2017Article
- Inhibition of Wnt/β-catenin signaling suppresses bleomycin-induced pulmonary fibrosis by attenuating the expression of TGF-β1 and FGF-2.Experimental and molecular pathology · 2016Article
- Chemical regulators of epithelial plasticity reveal a nuclear receptor pathway controlling myofibroblast differentiation.Scientific reports · 2016Article
- Mechanisms of TGFβ-Induced Epithelial-Mesenchymal Transition.Journal of clinical medicine · 2016Review
- Inhibitory effects of PPARγ ligands on TGF-β1-induced CTGF expression in cat corneal fibroblasts.Experimental eye research · 2015Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
Peroxisome proliferator activated receptor γ (PPARγ) agonists are effective antifibrotic agents in a number of tissues. Effects of these agents on epithelial-mesenchymal transition (EMT) of primary alveolar epithelial cells (AEC) and potential mechanisms underlying effects on EMT have not been well delineated. We examined effects of troglitazone, a synthetic PPARγ agonist, on transforming growth factor (TGF)-β1-induced EMT in primary rat AEC and an alveolar epithelial type II (AT2) cell line (RLE-6TN). TGF-β1 (2.5 ng/mL) induced EMT in both cell types, as evidenced by acquisition of spindle-like morphology, increased expression of the mesenchymal marker α-smooth muscle actin (α-SMA) and downregulation of the tight junctional protein zonula occludens-1 (ZO-1). Concurrent treatment with troglitazone (or rosiglitazone), ameliorated effects of TGF-β1. Furthermore, following stimulation with TGF-β1 for 6 days, troglitazone reversed EMT-related morphological changes and restored both epithelial and mesenchymal markers to control levels. Treatment with GW9662 (an irreversible PPARγ antagonist), or overexpression of a PPARγ dominant negative construct, failed to inhibit these effects of troglitazone in AEC. Troglitazone not only attenuated TGF-β1-induced phosphorylation of Akt and glycogen synthase kinase (GSK)-3β, but also inhibited nuclear translocation of β-catenin, phosphorylation of Smad2 and Smad3 and upregulation of the EMT-associated transcription factor SNAI1. These results demonstrate inhibitory actions of troglitazone on TGF-β1-induced EMT in AEC via a PPARγ-independent mechanism likely through inhibition of β-catenin-dependent signaling downstream of TGF-β1, supporting a role for interactions between TGF-β and Wnt/β-catenin signaling pathways in EMT.
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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.