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Lipopolysaccharide increases Aquaporin-5 in human lung epithelial cell via post-transcriptional mechanism(s)

Akira Ohinata ; Yoichiro Isohama ; Joji Nomura ; Kazufumi Nagai ; Akinori Hisatsue ; Takeshi Miyata

Journal of Pharmacological Sciences, 2003, Vol.91 (suppl.2), p.254-254 [Periódico revisado por pares]

The Japanese Pharmacological Society

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  • Título:
    Lipopolysaccharide increases Aquaporin-5 in human lung epithelial cell via post-transcriptional mechanism(s)
  • Autor: Akira Ohinata ; Yoichiro Isohama ; Joji Nomura ; Kazufumi Nagai ; Akinori Hisatsue ; Takeshi Miyata
  • É parte de: Journal of Pharmacological Sciences, 2003, Vol.91 (suppl.2), p.254-254
  • Descrição: Progress of lung inflammation can cause aberrance of water clearance such as increasing of mucus viscosity and lung edema. A water channel aquaporin-5 (AQP-5), which is expressed in epithelial cells at submucosal glands and alveoli, facilitates water movement in the distal lung. To investigate the possibility that change in the level of AQP- 5 is associated with bacterial infection and the abnormality of lung water flux, we examined the effect of lipopolysaccharide (LPS) on AQP-5 expression in A549 lung epithelial cells. In immunoblot analysis, AQP-5 protein level was increased after 24h treatment of LPS (10 μg/ml) to 3-fold of control level. This increase was dependent on concentration of LPS (1 to 10 μg/ml) and on incubation time (6-24h). To clarify this mechanism, we cloned the 5'-flanking region (1. 8 kb) of human AQP-5 gene and examined the effect of LPS on human AQP-5 promoter activity in A549 cells. However, LPS failed to increase AQP-5 promoter activity. These results suggested that AQP-5 protein expression in lung is up-regulated by LPS through post-transcriptional mechanism(s). We, therefore, assume that the increase in AQP-5 may be associated with the formation of pulmonary edema after bacterial infection.
  • Editor: The Japanese Pharmacological Society
  • Idioma: Japonês

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