Publication | Open Access
Expression and function of aquaporin-1 in hyperoxia-exposed alveolar epithelial type II cells
12
Citations
24
References
2014
Year
Acute Lung InjuryLung CellsInflammatory Lung DiseaseLung InflammationPulmonary Alveolar ProteinosisCellular PhysiologyOxidative StressInflammationPulmonary PharmacologyCell SignalingOsmoregulationMolecular PhysiologyPulmonary CirculationOsmotic StressHypoxia (Medicine)Gene Expression RegulationMembrane BiologyCell BiologyHyperoxic Lung InjuryPhysiologyPulmonary PhysiologyLung MechanicsMedicine
The aim of the present study was to investigate water transport dysfunction in alveolar epithelial type II cells (AECII), which were exposed to hyperoxia, and to investigate the mechanism of pulmonary edema resulting from hyperoxic lung injury. The lung cells of newborn rats were isolated for primary cell culture and divided into control and experimental groups. The control and experimental group cells were placed into a normoxic incubator (oxygen volume fraction, 0.21) or hyperoxic incubator (oxygen volume fraction, 0.9), respectively. Twenty‑four, 48 and 72 h after cell attachment, the gene transcription and protein expression levels of aquaporin‑1 (AQP1) were detected via quantitative polymerase chain reaction and western blot analysis. Flow cytometry was conducted to detect the volume of the cells in the experimental and control groups. In the present study, it was identified that AQP1 expression and cell volume were greater in the experimental group when compared with the control group. Thus, hyperoxia may disturb the gene expression regulation of AQP1 in AECII, resulting in water transport dysfunction. This may be one of the mechanisms underlying pulmonary edema caused by hyperoxic lung injury.
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