ArticleExperimental and therapeutic medicine2014
Expression and function of aquaporin-1 in hyperoxia-exposed alveolar epithelial type II cells.
Article in Experimental and therapeutic medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Dynamic Changes in Serum Aquaporin-1 and Aquaporin-5 in Transient Tachypnea of the Newborn.International journal of molecular sciences · 2026Article
- Understanding the relationship between lung GABABMC pulmonary medicine · 2026Article
- Aquaporins: a novel perspective in the treatment of lung diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Effects of Antioxidants in Human Milk on Bronchopulmonary Dysplasia Prevention and Treatment: A Review.Frontiers in nutrition · 2022Review
- Extrinsic Calcitonin Gene-Related Peptide Inhibits Hyperoxia-Induced Alveolar Epithelial Type II Cells Apoptosis, Oxidative Stress, and Reactive Oxygen Species (ROS) Production by Enhancing Notch 1 and Homocysteine-Induced Endoplasmic Reticulum Protein (HERP) Expression.Medical science monitor : international medical journal of experimental and clinical research · 2017Article
- Caveolin-1 regulates the expression of tight junction proteins during hyperoxia-induced pulmonary epithelial barrier breakdown.Respiratory research · 2016Article
- Wnt3a Mediates the Inhibitory Effect of Hyperoxia on the Transdifferentiation of AECIIs to AECIs.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2015Article
- Aquaporins in lung health and disease: Emerging roles, regulation, and clinical implications.Respiratory medicineReview
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Authors and funding
3 authors.
Funding
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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.
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