Document Detail


Clcn2 encodes the hyperpolarization-activated chloride channel in the ducts of mouse salivary glands.
MedLine Citation:
PMID:  18801913     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Victor G Romanenko; Tetsuji Nakamoto; Marcelo A Catalán; Mireya Gonzalez-Begne; George J Schwartz; Yasna Jaramillo; Francisco V Sepúlveda; Carlos D Figueroa; James E Melvin
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2008-09-18
Journal Detail:
Title:  American journal of physiology. Gastrointestinal and liver physiology     Volume:  295     ISSN:  0193-1857     ISO Abbreviation:  Am. J. Physiol. Gastrointest. Liver Physiol.     Publication Date:  2008 Nov 
Date Detail:
Created Date:  2008-11-06     Completed Date:  2009-01-06     Revised Date:  2013-06-05    
Medline Journal Info:
Nlm Unique ID:  100901227     Medline TA:  Am J Physiol Gastrointest Liver Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  G1058-67     Citation Subset:  IM    
Affiliation:
Center for Oral Biology, Univ. of Rochester Medical Center, Rochester, NY 14642, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Chloride Channels / genetics,  metabolism*
Cystic Fibrosis Transmembrane Conductance Regulator / metabolism
Electrophysiology
Epithelial Cells / metabolism
Gene Expression Regulation / physiology*
Mice
Mice, Knockout
Salivary Glands / cytology,  metabolism*
Sodium Chloride / metabolism
Time
Grant Support
ID/Acronym/Agency:
DE08921/DE/NIDCR NIH HHS; DE09692/DE/NIDCR NIH HHS; T32 DE07202/DE/NIDCR NIH HHS
Chemical
Reg. No./Substance:
0/Chloride Channels; 0/ClC-2 chloride channels; 126880-72-6/Cystic Fibrosis Transmembrane Conductance Regulator; 7647-14-5/Sodium Chloride
Comments/Corrections

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