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Papers In Press, published online ahead of print February 9, 2001
Department of Molecular Genetics, Biochemistry & Microbiology, University of Cincinnati, Cincinnati, OH 45267-0524
Corresponding Author: anil.menon{at}uc.edu
Aquaporin 5 (AQP5), the major water channel expressed in alveolar, tracheal, and upper bronchial epithelium, is significantly down-regulated during pulmonary inflammation and edema. The mechanisms that underlie this decrease in AQP5 levels are therefore of considerable interest. Here we show that AQP5 expression in cultured lung epithelial cells is decreased two-fold at the mRNA level, and ten-fold at the protein level by the proinflammatory cytokine tumor necrosis factor
J. Biol. Chem, 10.1074/jbc.M100322200
Submitted on January 12, 2001
Revised on February 6, 2001
Accepted on February 8, 2001
Tumor necrosis factor-alpha inhibits aquaporin 5 expression in mouse lung epithelial cells
(TNF-). Treatment of murine lung epithelial cells (MLE-12) with TNF- results in a concentration- and time-dependent decrease in AQP5 mRNA and protein expression. Activation of the p55 TNF- receptor (TNFR1) with an agonist antibody is sufficient to cause decreased AQP5 expression, demonstrating that the TNF- effect is mediated through TNFR1. Inhibition of nuclear factor 
B (NF-B) translocation to the nucleus blocks the effect of TNF- on AQP5 expression, indicating activation of NF-B is required, while inhibition of extracellular signal-regulated (ERK) or p38 MAP kinases showed no effect. These data show that TNF- decreases AQP5 mRNA and protein expression, and that the molecular pathway for this effect involves TNFR1 and activated NF-B. The ability of inflammatory cytokines to decrease aquaporin expression may help explain the connection between inflammation and edema.
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