ArticleLife sciences2013
Hyperoxia and transforming growth factor β1 signaling in the post-ischemic mouse heart.
Article in Life sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- LncRNA nonnmmut065573 promotes post-myocardial infarction cardiac fibrosis and activates the TGF-β1/ZEB1 pathway.Cell regeneration (London, England) · 2026Article
- Cannabidiol Protects the Neonatal Mouse Heart from Hyperoxia-Induced Injury.International journal of molecular sciences · 2025Article
- Cardioprotective Effects of Bosentan in Rats Subjected to Lung Ischemia-Reperfusion Injury.Medicina (Kaunas, Lithuania) · 2025Article
- MnSOD Mimetics in Therapy: Exploring Their Role in Combating Oxidative Stress-Related Diseases.Antioxidants (Basel, Switzerland) · 2024Review
- Inhibition of TGF-β-Smad signaling attenuates hyperoxia-induced brain damage in newborn rats.International journal of clinical and experimental pathology · 2019Article
- Hypoxia-induced activin A diminishes endothelial cell vasculogenic activity.Journal of cellular and molecular medicine · 2018Article
- Hyperoxia promotes polarization of the immune response in ovalbumin-induced airway inflammation, leading to a TH17 cell phenotype.Immunity, inflammation and disease · 2015Article
- Using a non-invasive assessment of lung injury in a murine model of acute lung injury.BMJ open respiratory research · 2014Article
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
aimsFollowing ischemic injury, myocardial healing and remodeling occur with characteristic myofibroblast trans-differentiation and scar formation. The current study tests the hypothesis that hyperoxia and nitric oxide (NO) regulate TGF-β1 signaling in the post-ischemic myocardium. MAIN
methodsC57BL/6 wild-type (WT), endothelial and inducible nitric oxide synthase knockout (eNOS(-/-) and iNOS(-/-)) mice were subjected to 30-min left anterior descending coronary artery occlusion followed by reperfusion. Myocardial tissue oxygenation was monitored with electron paramagnetic resonance oximetry. Protein expressions of TGF-β1, receptor-activated small mothers against decapentaplegic homolog (Smad), p21 and α-smooth muscle actin (α-SMA) were measured with enzyme-linked immunosorbent assay (ELISA), Western immunoblotting, and immunohistochemical staining. KEY
findingsThere was a hyperoxic state in the post-ischemic myocardial tissue. Protein expressions of total and active TGF-β1, p-Smad2/3 over t-Smad2/3 ratio, p21, and α-SMA were significantly increased in WT mice compared to Sham control. Knockout of eNOS or iNOS further increased protein expression of these signals. The expression of α-SMA was more abundant in the infarct of eNOS(-/-) and iNOS(-/-) mice than WT mice. A protein band indicating nitration of TGF-β type-II receptor (TGFβRII) was observed from WT heart. Carbogen (95% O2 plus 5% CO2) treatment increased the ratio of p-Smad2/t-Smad2, which was inhibited by 10006329 EUK (EUK134) and sodium nitroprusside (SNP). In conclusion, hyperoxia up-regulated and NO/ONOO(-) inhibited cardiac TGF-β1 signaling and myofibroblast trans-differentiation. SIGNIFICANCE: These findings may provide new insights in myocardial infarct healing and repair.
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