ArticleTuberculosis and respiratory diseases2019
The Effects of Retinoic Acid and MAPK Inhibitors on Phosphorylation of Smad2/3 Induced by Transforming Growth Factor β1.
Article in Tuberculosis and respiratory diseases, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
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- JR5558 mice are a reliable model to investigate subretinal fibrosis.Scientific reports · 2024Article
- A New Potential Therapeutic Target for Cancer in Ubiquitin-Like Proteins-UBL3.International journal of molecular sciences · 2023Review
- Scorpion Venom Polypeptide Inhibits Pulmonary Epithelial-Mesenchymal Transition in Systemic Sclerosis-Interstitial Lung Disease Model Mice by Intervening TGF-Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Inhibition of epithelial-mesenchymal transition in retinal pigment epithelial cells by a retinoic acid receptor-α agonist.Scientific reports · 2021Article
- Article
- Molecular characterization of a toxicological tipping point during human stem cell differentiation.Reproductive toxicology (Elmsford, N.Y.) · 2020Article
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundTransforming growth factor β (TGF-β), retinoic acid (RA), p38 mitogen-activated protein kinase (MAPK), and MEK signaling play critical roles in cell differentiation, proliferation, and apoptosis. We investigated the effect of RA and the role of these signaling molecules on the phosphorylation of Smad2/3 (p-Smad2/3) induced by TGF-β1.
methodsA549 epithelial cells and CCD-11Lu fibroblasts were incubated and stimulated with or without all-trans RA (ATRA) and TGF-β1 and with MAPK or MEK inhibitors. The levels of p-Smad2/3 were analyzed by western blotting. For animal models, we studied three experimental mouse groups: control, bleomycin, and bleomycin+ATRA group. Changes in histopathology, lung injury score, and levels of TGF-β1 and Smad3 were evaluated at 1 and 3 weeks.
resultsWhen A549 cells were pre-stimulated with TGF-β1 prior to RA treatment, RA completely inhibited the p-Smad2/3. However, when A549 cells were pre-treated with RA prior to TGF-β1 stimulation, RA did not completely suppress the p-Smad2/3. When A549 cells were pre-treated with MAPK inhibitor, TGF-β1 failed to phosphorylate Smad2/3. In fibroblasts, p38 MAPK inhibitor suppressed TGF-β1-induced p-Smad2. In a bleomycin-induced lung injury mouse model, RA decreased the expression of TGF-β1 and Smad3 at 1 and 3 weeks.
conclusionRA had inhibitory effects on the phosphorylation of Smad induced by TGF-β1
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