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Article

Inhibition of the expression of aquaporin‑1 by RNA interference in pulmonary epithelial cells and its effects on water transport

  • Authors:
    • Qiuyue Zhang
    • Jianhua Fu
    • Xindong Xue
  • View Affiliations / Copyright

    Affiliations: Department of Pediatrics, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China, Department of Pediatrics, China Medical University Affiliated to Shengjing Hospital, Shenyang, Liaoning 110004, P.R. China
  • Pages: 281-286
    |
    Published online on: November 6, 2015
       https://doi.org/10.3892/mmr.2015.4519
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Abstract

In the present study, the effect of aquaporin‑1 (AQP1) on fluid transportation in pulmonary epithelial cells, and the role of AQP1 in alveolar fluid clearance were investigated to provide an experimental foundation to elucidate the pathogenesis of hyperoxic lung edema. An siRNA transfection technique was used to silence AQP1 in the A549 cell line. The transfected cells were randomized into a hyperoxia exposure and an air control group, with a negative control group set for each group. Cell volume was determined using flow cytometry, and Pf values were used to determine osmotic water permeability. Cell volume was found to be reduced in the AQP1‑silenced A549 cells, compared with the negative control group 72 h following air exposure. In addition, cell volume was reduced in the AQP1‑silenced A549 cells, compared with the negative control group 48 and 72 h following hyperoxia exposure. The osmotic water permeability of the AQP1‑silenced cells was reduced in the air control and hyperoxia exposure groups, compared with the negative control group 48 and 72 h following exposure. The volume and cell membrane osmotic water permeability of the A549 cells were reduced, compared with those in the control group following AQP1‑silencing, which indicated that the downregulation of AQP1 impedes extracellular to intracellular fluid transportation. Therefore, the disturbance in alveolar fluid clearance resulting from the downregulation of AQP1 following hyperoxia exposure may be one of the key mechanisms responsible for hyperoxic lung edema.
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Copy and paste a formatted citation
Spandidos Publications style
Zhang Q, Fu J and Xue X: Inhibition of the expression of aquaporin‑1 by RNA interference in pulmonary epithelial cells and its effects on water transport. Mol Med Rep 13: 281-286, 2016.
APA
Zhang, Q., Fu, J., & Xue, X. (2016). Inhibition of the expression of aquaporin‑1 by RNA interference in pulmonary epithelial cells and its effects on water transport. Molecular Medicine Reports, 13, 281-286. https://doi.org/10.3892/mmr.2015.4519
MLA
Zhang, Q., Fu, J., Xue, X."Inhibition of the expression of aquaporin‑1 by RNA interference in pulmonary epithelial cells and its effects on water transport". Molecular Medicine Reports 13.1 (2016): 281-286.
Chicago
Zhang, Q., Fu, J., Xue, X."Inhibition of the expression of aquaporin‑1 by RNA interference in pulmonary epithelial cells and its effects on water transport". Molecular Medicine Reports 13, no. 1 (2016): 281-286. https://doi.org/10.3892/mmr.2015.4519
Copy and paste a formatted citation
x
Spandidos Publications style
Zhang Q, Fu J and Xue X: Inhibition of the expression of aquaporin‑1 by RNA interference in pulmonary epithelial cells and its effects on water transport. Mol Med Rep 13: 281-286, 2016.
APA
Zhang, Q., Fu, J., & Xue, X. (2016). Inhibition of the expression of aquaporin‑1 by RNA interference in pulmonary epithelial cells and its effects on water transport. Molecular Medicine Reports, 13, 281-286. https://doi.org/10.3892/mmr.2015.4519
MLA
Zhang, Q., Fu, J., Xue, X."Inhibition of the expression of aquaporin‑1 by RNA interference in pulmonary epithelial cells and its effects on water transport". Molecular Medicine Reports 13.1 (2016): 281-286.
Chicago
Zhang, Q., Fu, J., Xue, X."Inhibition of the expression of aquaporin‑1 by RNA interference in pulmonary epithelial cells and its effects on water transport". Molecular Medicine Reports 13, no. 1 (2016): 281-286. https://doi.org/10.3892/mmr.2015.4519
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