Placental growth factor gene silencing mitigates the epithelial‑to‑mesenchymal transition via the p38 MAPK pathway in rats with hyperoxia‑induced lung injury.

Placental growth factor gene silencing mitigates the epithelial‑to‑mesenchymal transition via... 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. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Molecular medicine reports Pubmed

Placental growth factor gene silencing mitigates the epithelial‑to‑mesenchymal transition via the p38 MAPK pathway in rats with hyperoxia‑induced lung injury.

Molecular medicine reports, Volume 20 (6): 8 – Nov 22, 2019
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Placental growth factor gene silencing mitigates the epithelial‑to‑mesenchymal transition via the p38 MAPK pathway in rats with hyperoxia‑induced lung injury.

Molecular medicine reports, Volume 20 (6): 8 – Nov 22, 2019

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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DOI
10.3892/mmr.2019.10785

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.

Journal

Molecular medicine reportsPubmed

Published: Nov 22, 2019

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