Nitric oxide decreases cell surface expression of aquaporin-5 and membrane water permeability in lung epithelial cells.
Nitric oxide (NO) is implicated in the pathogenesis of lung inflammation and edema. In this study, the effects of nitric oxide (NO)-donors on membrane water permeability and cell surface expression of aquaporin-5 (AQP5) in mouse lung epithelial cells were examined. NO-donors, GSNO and NOC-18 decreased cell surface expression of AQP5, concentration- and time-dependently, whereas they did not affect the amount of AQP5 in whole cell lysates. The membrane water permeability of cells was also decreased by treatment with NO-donors. The decrease in cell surface AQP5 by NO was abolished by simultaneous treatment with methyl-beta-cyclodextrin, but not with ODQ, an inhibitor of the cGMP-dependent pathway. In addition, immunocytochemistry with anti-AQP5 indicated that NO changed AQP5 localization from the plasma membrane to the intracellular fraction. These data indicate that NO stimulates AQP5 internalization from the plasma membrane through a cGMP-independent mechanism, and decreases membrane water permeability.
Nagai
Kazufumi
K
Department of Chemico-Pharmacological Sciences, Graduate School of Pharmaceutical Sciences, Kumamoto University, 5-1 Oe-honmachi, Kumamoto 862-0973, Japan.
Watanabe
Megumi
M
Seto
Mayumi
M
Hisatsune
Akinori
A
Miyata
Takeshi
T
Isohama
Yoichiro
Y
D000818:Animals; D051402:Aquaporin 5 / Q000037:antagonists & inhibitors* / Q000096:biosynthesis; D002460:Cell Line; D002463:Cell Membrane Permeability / Q000502:physiology*; D008168:Lung / Q000166:cytology / Q000378:metabolism*; D008565:Membrane Proteins / Q000037:antagonists & inhibitors* / Q000378:metabolism; D051379:Mice; D009569:Nitric Oxide / Q000502:physiology*; D020545:Respiratory Mucosa / Q000166:cytology / Q000378:metabolism*; D014867:Water / Q000378:metabolism*
D051402:Aquaporin 5; D008565:Membrane Proteins; D014867:Water; D009569:Nitric Oxide