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

Autor: Liang Zhang, Shuang Zhao, Hongmin Wu, Gang Luo
Jazyk: angličtina
Rok vydání: 2019
Předmět:
0301 basic medicine
MAPK/ERK pathway
Placental growth factor
Male
Cancer Research
placental growth factor
Epithelial-Mesenchymal Transition
Lung injury
Hyperoxia
Biochemistry
p38 Mitogen-Activated Protein Kinases
Rats
Sprague-Dawley
03 medical and health sciences
0302 clinical medicine
Pregnancy
Pulmonary fibrosis
bronchopulmonary dysplasia
Genetics
medicine
Gene silencing
hyperoxia-induced lung injury
Animals
Epithelial–mesenchymal transition
Gene Silencing
Molecular Biology
Lung
Placenta Growth Factor
Zinc Finger E-box Binding Homeobox 2
Chemistry
p38 mitogen-activated protein kinase
Vascular Endothelial Growth Factor Family
Articles
Lung Injury
respiratory system
medicine.disease
Cadherins
respiratory tract diseases
Rats
Disease Models
Animal
030104 developmental biology
Oncology
030220 oncology & carcinogenesis
Alveolar Epithelial Cells
Cancer research
Molecular Medicine
Female
epithelial-to-mesenchymal transition
medicine.symptom
Zdroj: Molecular Medicine Reports
ISSN: 1791-3004
1791-2997
Popis: 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.
Databáze: OpenAIRE
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