ArticleBMC pulmonary medicine2019
Effects of C/EBPα overexpression on alveolar epithelial type II cell proliferation, apoptosis and surfactant protein-C expression after exposure to hyperoxia.
Article in BMC pulmonary medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 11 citations in OpenAlex.
- Tfcp2l1 participates in paternal vitamin D deficiency-induced fetal lung maldevelopment in mice.Genes & nutrition · 2026Article
- IRF4-mediated Treg phenotype switching can aggravate hyperoxia-induced alveolar epithelial cell injury.BMC pulmonary medicine · 2024Article
- Mechanism of Adipose-Derived Mesenchymal Stem Cell-Derived Extracellular Vesicles Carrying miR-21-5p in Hyperoxia-Induced Lung Injury.Stem cell reviews and reports · 2022Article
- Sumoylation of CCAAT-enhancer-binding protein α inhibits lung differentiation in Bronchopulmonary Dysplasia model rats.Journal of cellular and molecular medicine · 2020Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundThis study aims to investigate the effects of CCAAT/enhancer binding protein alpha (C/EBPα) overexpression on cell proliferation, apoptosis and surfactant protein-C(SP-C) in alveolar epithelial type II (AEC II) cells after exposure to hyperoxia.
methodspcDNA3.1(+)-C/EBPα plasmid or air-empty vector were transfected into AEC II cells with or without hyperoxia. AEC II cells were divided into air group, air+pcDNA3.1-C/EBPα group, air-empty vector group, hyperoxia group, hyperoxia+pcDNA3.1-C/EBPα group, and hyperoxia-empty vector group. Cell proliferation was analyzed using Cell Counting Kit-8. The mRNA level and protein expression were measured using PCR and Western blot techniques, respectively. The cell cycle and apoptosis were analyzed using flow cytometry.
resultsAfter 48 h of post-transfection, significantly higher protein expression of C/EBPα was observed in the C/EBPα transfection group with or without hyperoxia compared to the others (P < 0.05). Compared to the air group, hyperoxia decreased cell proliferation, increased apoptosis, decreased SP-C expression, decreased percentage of cells in G1 phase, and increased percentage of cells in the S and G2 phases (P < 0.05); however, reversed by C/EBPα transfection (P < 0.05). No significant changes were observed in cell proliferation, SP-C expression, and apoptosis rates in the C/EBPα transfection group as compared to the controls air-empty vector group.
conclusionC/EBPα overexpression significantly upregulates the expression of SP-C, promotes cell proliferation, and inhibits apoptosis in AEC II cells after exposure to hyperoxia. Hence, this data suggests that C/EBPα overexpression may reverse the damage and exert a protective role in hyperoxia-induced lung injury.
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