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Received April 5, 2002
Accepted after revision August 28, 2002
1 Center for Oral Biology in the Aab Institute of Biomedical Sciences and Department of Pharmacology and Physiology, University of Rochester Medical Center, Rochester, NY 14642, USA
2 Department of Pharmacology and Physiology, University of Rochester Medical Center, Rochester, NY 14642, USA
3 Center for Oral Biology in the Aab Institute of Biomedical Sciences, University of Rochester Medical Center, Rochester, NY 14642, USA
4 Department of Pediatrics, University of Iowa, Iowa City, IA 52242, USA
5 Center for Oral Biology, University of Rochester, Medical Center Box 611, 601 Elmwood Avenue, Rochester, New York 14642, USA
* To whom correspondence should be addressed. E-mail: james-melvin{at}urmc.rochester.edu.
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.
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