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Updated: Sep 21, 2026
Modeling Hypoxia/Reoxygenation Injury in Proximal Tubular Epithelial Cells
Published on: November 21, 2025
LncRNA-NEF regulated the hyperoxia-induced injury of lung epithelial cells by FOXA2
Mei Mei1, Jing Nie1, Huawei Sun1
1The First Affiliated Hospital of Jms University Jiamusi 154000, Heilongjiang Province, China.
Introduction:
Hyperoxia-induced injury is a common form of damage in lung tissues, which could lead to bronchopulmonary dysplasia (BPD) in newborns. Recent studies have discovered that FOXA2 played a substantial role in protecting lung tissues from various injuries and lncRNA-NEF could activate the expression of FOXA2. However, it is unclear whether lncRNA-NEF could alleviate hyperoxia-caused damage of lung tissues by activating FOXA2.
Material And Methods:
In this study, we used the lentivirus to establish the lncRNA-NEF overexpression RLE-6TN and MLE-12 cells. After that, the lentivirus was also used to knockdown the expression of FOXA2 in the two lncRNA-NEF overexpression cells. ELISA was performed to detect the levels of TNF-α, IL-1β and IL-6. The production of ROS, SOD, MDA and LDH was determined with the commercial kits. The apoptosis rates of these cells were measured with the flow cytometry.
Results:
The secretion of TNF-α, IL-1β and IL-6 was inhibited in RLE-6TN and MLE-12 cells after the overexpression of lncRNA-NEF. Furthermore, the production of ROS, MDA and LDH was also suppressed after the upregulation of lncRNA-NEF. The promotion of lncRNA-NEF also restricted the hyperoxia-induced apoptosis. However, the knockdown of FOXA2 abolished all the inhibitory effects exerted by lncRNA-NEF.
Conclusion:
LncRNA-NEF regulated hyperoxia-caused inflammatory response, oxidative damage and apoptosis of RLE-6TN and MLE-12 cells by affecting the expression of FOXA2.
