Secretion and cell volume regulation by salivary acinar cells from mice lacking expression of the Clcn3 Cl- channel gene

Jorge Arreola; Ted Begenisich; Keith Nehrke; Ha‐Van  Nguyen; Keerang Park; Linda Richardson; Baoli Yang; Brian C Schutte; Fred S Lamb; James E Melvin

doi:10.1113/jphysiol.2002.021980

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Secretion and cell volume regulation by salivary acinar cells from mice lacking expression of the Clcn3 Cl- channel gene

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Secretion and cell volume regulation by salivary acinar cells from mice lacking expression of the Clcn3 Cl- channel gene

Jorge Arreola, Ted Begenisich, Keith Nehrke, Ha‐Van Nguyen, Keerang Park, Linda Richardson, Baoli Yang, Brian C Schutte, Fred S Lamb and James E Melvin

Journal of Physiology-London, Vol.545(1), pp.207-216

11/15/2002

DOI: 10.1113/jphysiol.2002.021980

PMCID: PMC2290643

PMID: 12433961

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Abstract

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 Ca2+‐calmodulin‐dependent protein kinase II; however, the magnitude of the Ca2+‐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.

Obstetrics and Gynecology

Details

Title: Subtitle: Secretion and cell volume regulation by salivary acinar cells from mice lacking expression of the Clcn3 Cl- channel gene
Creators: Jorge Arreola
Ted Begenisich
Keith Nehrke
Ha‐Van Nguyen
Keerang Park
Linda Richardson
Baoli Yang - University of Iowa
Brian C Schutte
Fred S Lamb
James E Melvin - University of Rochester Medical Center
Resource Type: Journal article
Publication Details: Journal of Physiology-London, Vol.545(1), pp.207-216
DOI: 10.1113/jphysiol.2002.021980
PMID: 12433961
PMCID: PMC2290643
NLM abbreviation: J Physiol
ISSN: 0022-3751
Grant note: This work was supported in part by National Institutes of Health Grants DE09692 and DE13539 (J.E.M).
Language: English
Date published: 11/15/2002
Academic Unit: BioVentures Center; Obstetrics and Gynecology
Record Identifier: 9983557427902771

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