JBC Anatrace, Inc.

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Originally published In Press as doi:10.1074/jbc.M100322200 on February 9, 2001

J. Biol. Chem., Vol. 276, Issue 22, 18657-18664, June 1, 2001
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
276/22/18657    most recent
M100322200v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Towne, J. E.
Right arrow Articles by Menon, A. G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Towne, J. E.
Right arrow Articles by Menon, A. G.
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

Tumor Necrosis Factor-alpha Inhibits Aquaporin 5 Expression in Mouse Lung Epithelial Cells*

Jennifer E. TowneDagger §, Carissa M. KraneDagger , Cindy J. Bachurski, and Anil G. MenonDagger ||

From the Dagger  Department of Molecular Genetics, Biochemistry, and Microbiology, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267-0524 and the  Division of Pulmonary Biology, Children's Hospital Medical Center, Cincinnati, Ohio 45229

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 2-fold at the mRNA level and 10-fold at the protein level by the proinflammatory cytokine tumor necrosis factor alpha  (TNF-alpha ). Treatment of murine lung epithelial cells (MLE-12) with TNF-alpha results in a concentration- and time-dependent decrease in AQP5 mRNA and protein expression. Activation of the p55 TNF-alpha receptor (TNFR1) with an agonist antibody is sufficient to cause decreased AQP5 expression, demonstrating that the TNF-alpha effect is mediated through TNFR1. Inhibition of nuclear factor kappa B (NF-kappa B) translocation to the nucleus blocks the effect of TNF-alpha on AQP5 expression, indicating that activation of NF-kappa B is required, whereas inhibition of extracellular signal-regulated or p38 mitogen-activated protein kinases showed no effect. These data show that TNF-alpha decreases AQP5 mRNA and protein expression and that the molecular pathway for this effect involves TNFR1 and activated NF-kappa B. The ability of inflammatory cytokines to decrease aquaporin expression may help explain the connection between inflammation and edema.

* This work was supported in part by Grants RO1 DE138283 (to A. G. M.) and RO1 HL60907 from the National Institutes of Health (to C. J. B.), Grant HL61781 from the NHLBI Program of Excellence in Molecular Biology of Heart and Lung, National Institutes of Health (to A. G. M.), and a new investigator grant from this program (to C. M. K.), and by the Caroline Halfter-Spahn Trust.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

§ Supported in part by a predoctoral fellowship from the University of Cincinnati and an Albert J. Ryan Foundation fellowship.

|| To whom correspondence should be addressed: Dept. of Molecular Genetics, Biochemistry, and Microbiology, University of Cincinnati College of Medicine, 231 Albert Sabin Way, 3110 MSB, P. O. Box 670524, Cincinnati, OH 45267-0524. Tel.: 513-558-5534; Fax: 513-558-1885; E-mail: Anil.Menon@UC.edu.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?


This article has been cited by other articles:


Home page
 Am. J. Physiol. Gastrointest. Liver Physiol.Home page
G. L. Lehmann, F. I. Carreras, L. R. Soria, S. A. Gradilone, and R. A. Marinelli
LPS induces the TNF-{alpha}-mediated downregulation of rat liver aquaporin-8: role in sepsis-associated cholestasis
Am J Physiol Gastrointest Liver Physiol, February 1, 2008; 294(2): G567 - G575.
[Abstract] [Full Text] [PDF]

Home page
 Proc. Natl. Acad. Sci. USAHome page
V. K. Sidhaye, A. D. Guler, K. S. Schweitzer, F. D'Alessio, M. J. Caterina, and L. S. King
Transient receptor potential vanilloid 4 regulates aquaporin-5 abundance under hypotonic conditions
PNAS, March 21, 2006; 103(12): 4747 - 4752.
[Abstract] [Full Text] [PDF]

Home page
 EndocrinologyHome page
J. Anderson, N. Brown, M. S. Mahendroo, and J. Reese
Utilization of Different Aquaporin Water Channels in the Mouse Cervix during Pregnancy and Parturition and in Models of Preterm and Delayed Cervical Ripening
Endocrinology, January 1, 2006; 147(1): 130 - 140.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
V. Sidhaye, J. D. Hoffert, and L. S. King
cAMP Has Distinct Acute and Chronic Effects on Aquaporin-5 in Lung Epithelial Cells
J. Biol. Chem., February 4, 2005; 280(5): 3590 - 3596.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
F. Yang, J. D. Kawedia, and A. G. Menon
Cyclic AMP Regulates Aquaporin 5 Expression at Both Transcriptional and Post-transcriptional Levels through a Protein Kinase A Pathway
J. Biol. Chem., August 22, 2003; 278(34): 32173 - 32180.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
C. D. N. Cher, A. Armugam, R. Lachumanan, M.-W. Coghlan, and K. Jeyaseelan
Pulmonary Inflammation and Edema Induced by Phospholipase A2: GLOBAL GENE ANALYSIS AND EFFECTS ON AQUAPORINS AND Na+/K+-ATPase
J. Biol. Chem., August 15, 2003; 278(33): 31352 - 31360.
[Abstract] [Full Text] [PDF]

Home page
 J. Appl. Physiol.Home page
Z. Borok and A. S. Verkman
Lung Edema Clearance: 20 Years of Progress: Invited Review: Role of aquaporin water channels in fluid transport in lung and airways
J Appl Physiol, December 1, 2002; 93(6): 2199 - 2206.
[Abstract] [Full Text] [PDF]

Home page
 Proc. Natl. Acad. Sci. USAHome page
C. M. Krane, C. N. Fortner, A. R. Hand, D. W. McGraw, J. N. Lorenz, S. E. Wert, J. E. Towne, R. J. Paul, J. A. Whitsett, and A. G. Menon
Aquaporin 5-deficient mouse lungs are hyperresponsive to cholinergic stimulation
PNAS, November 9, 2001; (2001) 231273398.
[Abstract] [Full Text] [PDF]

Home page
 Proc. Natl. Acad. Sci. USAHome page
C. M. Krane, C. N. Fortner, A. R. Hand, D. W. McGraw, J. N. Lorenz, S. E. Wert, J. E. Towne, R. J. Paul, J. A. Whitsett, and A. G. Menon
Aquaporin 5-deficient mouse lungs are hyperresponsive to cholinergic stimulation
PNAS, November 20, 2001; 98(24): 14114 - 14119.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 All ASBMB Journals   Molecular and Cellular Proteomics 
 Journal of Lipid Research   ASBMB Today 
Copyright © 2001 by the American Society for Biochemistry and Molecular Biology.