ArticleFree radical biology & medicine2011
Nox2-derived ROS in PPARγ signaling and cell-cycle progression of lung alveolar epithelial cells.
Article in Free radical biology & medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 35 citations in OpenAlex.
- Hypoxia-injured pulmonary vascular targeting and microenvironment-responsive nanoparticle to treat hypoxic pulmonary hypertension.Journal of nanobiotechnology · 2026Article
- NADPH oxidases: redox regulation of cell homeostasis and disease.Physiological reviews · 2025Review
- Harnessing peroxisome proliferator-activated receptor γ agonists to induce Heme Oxygenase-1: a promising approach for pulmonary inflammatory disorders.Cell communication and signaling : CCS · 2024Review
- NOX-2 Inhibitors may be Potential Drug Candidates for the Management of COVID-19 Complications.Current drug research reviews · 2024Review
- PPAR-γ Agonist GW1929 Targeted to Macrophages with Dendrimer-Graphene Nanostars Reduces Liver Fibrosis and Inflammation.Pharmaceutics · 2023Article
- Deciphering the Heterogeneity of Mitochondrial Functions During Hematopoietic Lineage Differentiation.Stem cell reviews and reports · 2022Article
- Expression and enhancement of FABP4 in septoclasts of the growth plate in FABP5-deficient mouse tibiae.Histochemistry and cell biology · 2021Article
- Redox-Mediated Mechanism of Chemoresistance in Cancer Cells.Antioxidants (Basel, Switzerland) · 2019Review
- Loss of Scribble confers cisplatin resistance during NSCLC chemotherapy via Nox2/ROS and Nrf2/PD-L1 signaling.EBioMedicine · 2019Article
- Haem oxygenase-1 up-regulation by rosiglitazone via ROS-dependent Nrf2-antioxidant response elements axis or PPARγ attenuates LPS-mediated lung inflammation.British journal of pharmacology · 2018Article
- Rosiglitazone inhibits PM2.5-induced cytotoxicity in human lung epithelial A549 cells.Annals of translational medicine · 2018Article
- Glucose-6-phosphate dehydrogenase inhibition attenuates acute lung injury through reduction in NADPH oxidase-derived reactive oxygen species.Clinical and experimental immunology · 2018Article
- The matricellular protein TSP1 promotes human and mouse endothelial cell senescence through CD47 and Nox1.Science signaling · 2017Article
- BL-038, a Benzofuran Derivative, Induces Cell Apoptosis in Human Chondrosarcoma Cells through Reactive Oxygen Species/Mitochondrial Dysfunction and the Caspases Dependent Pathway.International journal of molecular sciences · 2016Article
- Oxidative stress, redox signalling and endothelial dysfunction in ageing-related neurodegenerative diseases: a role of NADPH oxidase 2.British journal of clinical pharmacology · 2014Review
- NADPH oxidases in lung health and disease.Antioxidants & redox signaling · 2014Review
- Protection against LPS-induced acute lung injury by a mechanism-based inhibitor of NADPH oxidase (type 2).American journal of physiology. Lung cellular and molecular physiology · 2014Article
- Redox control of inflammation in macrophages.Antioxidants & redox signaling · 2013Review
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Authors and funding
5 authors at 1 institution in 1 country.
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Abstract
Reactive oxygen species (ROS) play important roles in peroxisome proliferator-activated receptor γ (PPARγ) signaling and cell-cycle regulation. However, the PPARγ redox-signaling pathways in lung alveolar epithelial cells remain unclear. In this study, we investigated the in vivo and in vitro effects of PPARγ activation on the levels of lung ROS production and cell-cycle progression using C57BL/6J wild-type and Nox2 knockout mice (n=10) after intraperitoneal injection of a selective PPARγ agonist (GW1929, 5 mg/kg body wt, daily) for 14 days. Compared to vehicle-treated mice, GW1929 increased significantly the levels of ROS production in wild-type lungs, and this was accompanied by significant up-regulation of PPARγ, Nox2, PCNA, and cyclin D1 and phosphorylation of ERK1/2 and p38MAPK. These effects were absent in Nox2 knockout mice. In cultured alveolar epithelial cells, GW1929 (5 μM for 24 h) increased ROS production and promoted cell-cycle progression from G0/G1 into S and G2/M phases, and these effects were abolished by (1) adding a PPARγ antagonist (BADGE, 1 μM), (2) knockdown of PPARγ using siRNA, or (3) knockout of Nox2. In conclusion, PPARγ activation through Nox2-derived ROS promotes cell-cycle progression in normal mouse lungs and in cultured normal alveolar epithelial cells.
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Registered trials
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