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.

Highlights

  • Hyperoxia-induced lung injury (HILI) is one of the major causes of death and morbidity in premature infants, especially those with extremely low birth weight [1, 2]

  • CCAAT/enhancer binding protein alpha (C/EBPα) gene-deficient mature rats are sensitive to hyperoxia, following which, severe lung inflammation and decreased expression of surfactant protein-B (SP-B) are observed in mice, thereby indicating that C/EBPα exerts a protective role in hyperoxia-induced lung injury [18, 19]

  • Overexpression of C/EBPα improves the secretion of surfactant protein-C (SP-C) in AEC Alveolar epithelial type II (II) after exposure to hyperoxia Previous study showed that the expression of C/EBPα can be improved after a short period of exposure to hyperoxia, since it exerts a protective regulatory effect on the pulmonary function during the early stage of hyperoxia stress

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Summary

Introduction

Hyperoxia-induced lung injury (HILI) is one of the major causes of death and morbidity in premature infants, especially those with extremely low birth weight [1, 2]. C/EBPα gene-deficient mature rats are sensitive to hyperoxia, following which, severe lung inflammation and decreased expression of surfactant protein-B (SP-B) are observed in mice, thereby indicating that C/EBPα exerts a protective role in hyperoxia-induced lung injury [18, 19]. We investigated the effects of C/EBPα overexpression on AEC II cell proliferation, apoptosis, and surfactant protein-C (SP-C) after exposure to hyperoxia and lay a foundation to study the pathogenesis and the prevention of hyperoxia-induced lung injury. This 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

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