Abstract
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.
Highlights
Aquaporins (AQPs) are a family of hydrophobic transmembrane proteins that are selectively energized and impermeable to small molecules, which have been confirmed to exist in various entities, including bacteria, yeast and plants [1]
Previous studies have shown that following birth, moisture was rapidly absorbed in the alveoli of mammalian embryos to enable a transition to spontaneous breathing, whilst AQP1 expression simultaneously increased in the lung tissue [6]
Immunofluorescence of surfactant protein (SP)‐C and transmission electron microscopy (TEM; Olympus, Tokyo, Japan) were used to verify the Alveolar epithelial type II cells (AEC II) cells, in addition, the viability of cells was determined by trypan blue staining
Summary
Aquaporins (AQPs) are a family of hydrophobic transmembrane proteins that are selectively energized and impermeable to small molecules, which have been confirmed to exist in various entities, including bacteria, yeast and plants [1]. Various studies have demonstrated a complex network in the epithelium of the airway, which regulates water transportation, the studies indicated that six types of AQPs are expressed in the lungs [2,3]. Numerous studies from the 1990s have identified that water is involved in the process of cell metabolism and achieves transmembrane transport via AQPs, which are highly selective for water molecules. Previous studies have shown that following birth, moisture was rapidly absorbed in the alveoli of mammalian embryos to enable a transition to spontaneous breathing, whilst AQP1 expression simultaneously increased in the lung tissue [6]. A further study identified that the fluid transportation rate of the alveolar‐capillary system decreased significantly within an AQP1 knock-out animal [9,10]
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