ArticleThe Journal of physiology2002
Secretion and cell volume regulation by salivary acinar cells from mice lacking expression of the Clcn3 Cl- channel gene.
Article in The Journal of physiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 99 citations in OpenAlex.
- Review
- Notch signaling is a driver of glandular stem cell activity and regenerative migration after damage.The EMBO journal · 2026Article
- Excitotoxic neuronal death requires superoxide entry into neurons through volume-regulated anion channels.Science advances · 2025Article
- Ablation of TRPC3 disrupts CaScientific reports · 2023Article
- Chloride Channel-3 (ClC-3) Modifies the Trafficking of Leucine-Rich Repeat-Containing 8A (LRRC8A) Anion Channels.The Journal of membrane biology · 2023Article
- A Mathematical Model Supports a Key Role for Ae4 (Slc4a9) in Salivary Gland Secretion.Bulletin of mathematical biology · 2018Article
- ClC Channels and Transporters: Structure, Physiological Functions, and Implications in Human Chloride Channelopathies.Frontiers in pharmacology · 2017Review
- Ion channels in regulated cell death.Cellular and molecular life sciences : CMLS · 2016Review
- VRAC: molecular identification as LRRC8 heteromers with differential functions.Pflugers Archiv : European journal of physiology · 2016Review
- Biophysics and Physiology of the Volume-Regulated Anion Channel (VRAC)/Volume-Sensitive Outwardly Rectifying Anion Channel (VSOR).Pflugers Archiv : European journal of physiology · 2016Review
- Threonine532 phosphorylation in ClC-3 channels is required for angiotensin II-induced Cl(-) current and migration in cultured vascular smooth muscle cells.British journal of pharmacology · 2016Article
- ClC-3 Expression and Its Association with Hyperglycemia Induced HT22 Hippocampal Neuronal Cell Apoptosis.Journal of diabetes research · 2016Article
- Discovery of CLC transport proteins: cloning, structure, function and pathophysiology.The Journal of physiology · 2015Review
- Chloride channel-3 promotes tumor metastasis by regulating membrane ruffling and is associated with poor survival.Oncotarget · 2015Article
- Cl⁻ channels in smooth muscle cells.Pflugers Archiv : European journal of physiology · 2014Review
- Identification of key signaling molecules involved in the activation of the swelling-activated chloride current in human glioblastoma cells.The Journal of membrane biology · 2014Article
- Deorphanizing the human transmembrane genome: A landscape of uncharacterized membrane proteins.Acta pharmacologica Sinica · 2014Review
- Functional regulation of ClC-3 in the migration of vascular smooth muscle cells.Hypertension (Dallas, Tex. : 1979) · 2013Article
- Regulation of transport in the connecting tubule and cortical collecting duct.Comprehensive Physiology · 2012Review
- Ion channels and transporters [corrected] in cancer. 2. Ion channels and the control of cancer cell migration.American journal of physiology. Cell physiology · 2011Review
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
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 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.
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