ArticleMolecular medicine reports2019
Placental growth factor gene silencing mitigates the epithelial‑to‑mesenchymal transition via the p38 MAPK pathway in rats with hyperoxia‑induced lung injury.
Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Neonatal hyperoxia promotes macrophage senescence and lung injury via a p38MAPK-dependent secretome.American journal of respiratory cell and molecular biology · 2026Article
- Post-translational modifications and bronchopulmonary dysplasia.Frontiers in pediatrics · 2024Review
- Umbilical cord blood exosomes from very preterm infants with bronchopulmonary dysplasia aggravate lung injury in mice.Scientific reports · 2023Article
- NLRX1 knockdown attenuates pro-apoptotic signaling and cell death in pulmonary hyperoxic acute injury.Scientific reports · 2023Article
- The NMolecular cancer · 2022Article
- CFTR Correctors and Antioxidants Partially Normalize Lipid Imbalance but not Abnormal Basal Inflammatory Cytokine Profile in CF Bronchial Epithelial Cells.Frontiers in physiology · 2021Article
- Physical activity differentially regulates VEGF, PlGF, and their receptors in the human placenta.Physiological reports · 2021Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
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Abstract
Hyperoxia may cause pulmonary fibrosis in neonates and is characterized by the epithelial‑to‑mesenchymal transition (EMT) of alveolar epithelial cells. The placental growth factor (PLGF) gene is a member of the vascular endothelial growth factor family and is highly expressed in lung tissues that have been exposed to hyperoxia. The aim of the present study was to assess the role of PLGF in the EMT of lung tissue. Lung tissue exhibiting low PLGF expression was obtained by injecting rats exposed to hyperoxia with a PLGF‑silencing lentiviral plasmid. Western blot analysis and immunohistochemistry revealed that expression levels of the EMT‑related protein epithelial‑cadherin were increased, whereas its inhibitor protein zinc‑finger E‑box binding homeobox 2 was decreased in these rats. These data demonstrated that PLGF silencing may significantly mitigate hyperoxia‑induced EMT in rat lung tissue. Additionally, an increase in phosphorylated‑p38 MAPK protein expression indicated that PLGF may be able to regulate hyperoxia‑induced lung injury in rats via the p38 MAPK pathway.
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