Control of ion transport in mammalian airways by protease activated receptors type 2 (PAR-2)

Kunzelmann, Karl, Sun, Jane, Markovich, Daniel, Konig, Jens, Murle, Bettina, Mall, Marcus and Schreiber, Rainer (2005) Control of ion transport in mammalian airways by protease activated receptors type 2 (PAR-2). The FASEB Journal, 19 8: 969-970. doi:10.1096/fj.04-2469fje


Author Kunzelmann, Karl
Sun, Jane
Markovich, Daniel
Konig, Jens
Murle, Bettina
Mall, Marcus
Schreiber, Rainer
Title Control of ion transport in mammalian airways by protease activated receptors type 2 (PAR-2)
Journal name The FASEB Journal   Check publisher's open access policy
ISSN 0892-6638
1530-6860
Publication date 2005-06
Sub-type Article (original research)
DOI 10.1096/fj.04-2469fje
Volume 19
Issue 8
Start page 969
End page 970
Total pages 2
Place of publication Bethesda, MD, U.S.A.
Publisher Federation of American Societies for Experimental Biology
Collection year 2005
Language eng
Subject C1
270699 Physiology not elsewhere classified
730118 Organs, diseases and abnormal conditions not elsewhere classified
Abstract Protease-activated receptors (PARs) are widely distributed in human airways. They couple to G-proteins and are activated after proteolytic cleavage of the N terminus of the receptor. Evidence is growing that PAR subtype 2 plays a pivotal role in inflammatory airway diseases, such as allergic asthma or bronchitis. However, nothing is known about the effects of PAR-2 on electrolyte transport in the native airways. PAR-2 is expressed in airway epithelial cells, where they are activated by mast cell tryptase, neutrophil proteinase 3, or trypsin. Recent studies produced conflicting results about the functional consequence of PAR-2 stimulation. Here we report that stimulation of PAR-2 receptors in mouse and human airways leads to a change in electrolyte transport and a shift from absorption to secretion. Although PAR-2 appears to be expressed on both sides of the epithelium, only basolateral stimulation results in inhibition of amiloride sensitive Na+ conductance and stimulation of both luminal Cl- channels and basolateral K+ channels. The present data indicate that these changes occur through activation of phospholipase C and increase in intracellular Ca2+, which activates basolateral SK4 K+ channels and luminal Ca2+-dependent Cl- channels. In addition, the present data suggest a PAR-2 mediated release of prostaglandin E2, which may contribute to the secretory response. In conclusion, these results provide further evidence for a role of PAR-2 in inflammatory airway disease: stimulation of these receptors may cause accumulation of airway surface liquid, which, however, may help to flush noxious stimuli away from the affected airways. ©2005 FASEB
Keyword Biochemistry & molecular biology
Biology
Cell biology
Airway epithelium
Trypsin
Tryptase
Bronchial epithelial-cells
Cystic-fibrosis mouse
Guinea-pig
Cl-secretion
Inflammation
Expression
Mice
Inhibition
Modulation
Channels
Q-Index Code C1
Additional Notes FJ Express summary article (Abstract) published in print journal (pp. 969-970), full-text published in online version

 
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Created: Wed, 15 Aug 2007, 06:13:59 EST