Document Detail


Secretion and cell volume regulation by salivary acinar cells from mice lacking expression of the Clcn3 Cl- channel gene.
MedLine Citation:
PMID:  12433961     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Salivary gland acinar cells shrink when Cl(-) currents are activated following cell swelling induced by exposure to a hypotonic solution or in response to calcium-mobilizing agonists. The molecular identity of the Cl(-) channel(s) in salivary cells involved in these processes is unknown, although ClC-3 has been implicated in several tissues as a cell-volume-sensitive Cl(-) channel. We found that cells isolated from mice with targeted disruption of the Clcn3 gene undergo regulatory volume decrease in a fashion similar to cells from wild-type littermates. Consistent with a normal regulatory volume decrease response, the magnitude and the kinetics of the swell-activated Cl(-) currents in cells from ClC-3-deficient mice were equivalent to those from wild-type mice. It has also been suggested that ClC-3 is activated by Ca(2+)-calmodulin-dependent protein kinase II; however, the magnitude of the Ca(2+)-dependent Cl(-) current was unchanged in the Clcn3(-/-) animals. In addition, we observed that ClC-3 appeared to be highly expressed in the smooth muscle cells of glandular blood vessels, suggesting a potential role for this channel in saliva production by regulating blood flow, yet the volume and ionic compositions of in vivo stimulated saliva from wild-type and null mutant animals were comparable. Finally, in some cells ClC-3 is an intracellular channel that is thought to be involved in vesicular acidification and secretion. Nevertheless, the protein content of saliva was unchanged in Clcn3(-/-) mice. Our results demonstrate that the ClC-3 Cl(-) channel is not a major regulator of acinar cell volume, nor is it essential for determining the secretion rate and composition of saliva.
Authors:
Jorge Arreola; Ted Begenisich; Keith Nehrke; Ha-Van Nguyen; Keerang Park; Linda Richardson; Baoli Yang; Brian C Schutte; Fred S Lamb; James E Melvin
Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The Journal of physiology     Volume:  545     ISSN:  0022-3751     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  2002 Nov 
Date Detail:
Created Date:  2002-11-15     Completed Date:  2003-05-07     Revised Date:  2013-06-09    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  207-16     Citation Subset:  IM    
Affiliation:
Center for Oral Biology, Aab Institute of Biomedical Sciences, Department of Pharmacology and Physiology, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY 14642, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Calcium / physiology
Chloride Channels / deficiency*,  metabolism,  physiology
Electric Conductivity
Electrolytes / metabolism
Male
Mice
Mice, Knockout
Parotid Gland / cytology*,  metabolism*
Saliva / secretion
Salivary Proteins and Peptides / metabolism
Grant Support
ID/Acronym/Agency:
DE 09692/DE/NIDCR NIH HHS; DE 13539/DE/NIDCR NIH HHS
Chemical
Reg. No./Substance:
0/Chloride Channels; 0/ClC-3 channel; 0/Electrolytes; 0/Salivary Proteins and Peptides; 7440-70-2/Calcium
Comments/Corrections

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