ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2008
Clcn2 encodes the hyperpolarization-activated chloride channel in the ducts of mouse salivary glands.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 33 citations in OpenAlex.
- Review
- Salivary gland function, development, and regeneration.Physiological reviews · 2022Review
- Salivary gland proteins alterations in the diabetic milieu.Journal of molecular histology · 2021Review
- Sexual dimorphisms in the transcriptomes of murine salivary glands.FEBS open bio · 2019Article
- Systemic network for dietary inorganic phosphate adaptation among three organs.Pflugers Archiv : European journal of physiology · 2019Article
- Essential role of carbonic anhydrase XII in secretory gland fluid and HCO3 (-) secretion revealed by disease causing human mutation.The Journal of physiology · 2015Article
- Regulatory-auxiliary subunits of CLC chloride channel-transport proteins.The Journal of physiology · 2015Review
- Identification and characterization of the zebrafish ClC-2 chloride channel orthologs.Pflugers Archiv : European journal of physiology · 2015Article
- Ae4 (Slc4a9) Anion Exchanger Drives Cl- Uptake-dependent Fluid Secretion by Mouse Submandibular Gland Acinar Cells.The Journal of biological chemistry · 2015Article
- A fluid secretion pathway unmasked by acinar-specific Tmem16A gene ablation in the adult mouse salivary gland.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- A quantitative analysis of electrolyte exchange in the salivary duct.American journal of physiology. Gastrointestinal and liver physiology · 2012Article
- Extracellular Ca(2+) sensing in salivary ductal cells.The Journal of biological chemistry · 2012Article
- CFTR-mediated Cl(-) transport in the acinar and duct cells of rabbit lacrimal gland.Current eye research · 2012Article
- Changes of chloride channels in the lacrimal glands of a rabbit model of Sjögren syndrome.Cornea · 2012Article
- Functional characterization of a ClC-2-like Cl(-) conductance in surface epithelial cells of rat rectal colon.The Journal of membrane biology · 2010Article
- Tmem16A encodes the Ca2+-activated Cl- channel in mouse submandibular salivary gland acinar cells.The Journal of biological chemistry · 2010Article
- Inward-rectifier chloride currents in Reissner's membrane epithelial cells.Biochemical and biophysical research communications · 2010Article
- Cftr and ENaC ion channels mediate NaCl absorption in the mouse submandibular gland.The Journal of physiology · 2010Article
- ClC-2 regulation of intestinal barrier function: Translation of basic science to therapeutic target.Tissue barriersReview
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Transepithelial Cl(-) transport in salivary gland ducts is a major component of the ion reabsorption process, the final stage of saliva production. It was previously demonstrated that a Cl(-) current with the biophysical properties of ClC-2 channels dominates the Cl(-) conductance of unstimulated granular duct cells in the mouse submandibular gland. This inward-rectifying Cl(-) current is activated by hyperpolarization and elevated intracellular Cl(-) concentration. Here we show that ClC-2 immunolocalized to the basolateral region of acinar and duct cells in mouse salivary glands, whereas its expression was most robust in granular and striated duct cells. Consistent with this observation, nearly 10-fold larger ClC-2-like currents were observed in granular duct cells than the acinar cells obtained from submandibular glands. The loss of inward-rectifying Cl(-) current in cells from Clcn2(-/-) mice confirmed the molecular identity of the channel responsible for these currents as ClC-2. Nevertheless, both in vivo and ex vivo fluid secretion assays failed to identify significant changes in the ion composition, osmolality, or salivary flow rate of Clcn2(-/-) mice. Additionally, neither a compensatory increase in Cftr Cl(-) channel protein expression nor in Cftr-like Cl(-) currents were detected in Clcn2 null mice, nor did it appear that ClC-2 was important for blood-organ barrier function. We conclude that ClC-2 is the inward-rectifying Cl(-) channel in duct cells, but its expression is not apparently required for the ion reabsorption or the barrier function of salivary ductal epithelium.
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