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http://purl.uniprot.org/citations/22079595http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/22079595http://www.w3.org/2000/01/rdf-schema#comment"

Background & aims

The fluid secretion model predicts that intestinal obstruction disorders can be alleviated by promoting epithelial Cl(-) secretion. The adenosine 3',5'-cyclic monophosphate (cAMP)-activated anion channel CFTR mediates Cl(-)-dependent fluid secretion in the intestine. Although the role of the ClC-2 channel has not been determined in the intestine, this voltage-gated Cl(-) channel might compensate for the secretory defects observed in patients with cystic fibrosis and other chronic constipation disorders. We investigated whether mice that lack ClC-2 channels (Clcn2(-/-)) have defects in intestinal ion transport.

Methods

Immunolocalization and immunoblot analyses were used to determine the cellular localization and the amount of ClC-2 expressed in mouse early distal colon (EDC) and late distal colon (LDC). Colon sheets from wild-type and Clcn2(-/-) littermates were mounted in Ussing chambers to determine transepithelial bioelectrical parameters and Na(+), K(+), and Cl(-) fluxes.

Results

Expression of ClC-2 was higher in the basolateral membrane of surface cells in the EDC compared with the LDC, with little expression in crypts. Neither cAMP nor Ca(2+)-induced secretion of Cl(-) was affected in the EDC or LDC of Clcn2(-/-) mice, whereas the amiloride-sensitive short-circuit current was increased approximately 3-fold in Clcn2(-/-) EDC compared with control littermates. Conversely, electroneutral Na(+), K(+), and Cl(-) absorption was dramatically reduced in colons of Clcn2(-/-) mice.

Conclusions

Basolateral ClC-2 channels are required for colonic electroneutral absorption of NaCl and KCl. The increase in the amiloride-sensitive short-circuit current in Clcn2(-/-) mice revealed a compensatory mechanism that is activated in the colons of mice that lack the ClC-2 channel."xsd:string
http://purl.uniprot.org/citations/22079595http://purl.org/dc/terms/identifier"doi:10.1053/j.gastro.2011.10.037"xsd:string
http://purl.uniprot.org/citations/22079595http://purl.uniprot.org/core/author"Zhang Y."xsd:string
http://purl.uniprot.org/citations/22079595http://purl.uniprot.org/core/author"Sepulveda F.V."xsd:string
http://purl.uniprot.org/citations/22079595http://purl.uniprot.org/core/author"Melvin J.E."xsd:string
http://purl.uniprot.org/citations/22079595http://purl.uniprot.org/core/author"Flores C.A."xsd:string
http://purl.uniprot.org/citations/22079595http://purl.uniprot.org/core/author"Catalan M.A."xsd:string
http://purl.uniprot.org/citations/22079595http://purl.uniprot.org/core/author"Gonzalez-Begne M."xsd:string
http://purl.uniprot.org/citations/22079595http://purl.uniprot.org/core/date"2012"xsd:gYear
http://purl.uniprot.org/citations/22079595http://purl.uniprot.org/core/name"Gastroenterology"xsd:string
http://purl.uniprot.org/citations/22079595http://purl.uniprot.org/core/pages"346-354"xsd:string
http://purl.uniprot.org/citations/22079595http://purl.uniprot.org/core/title"Severe defects in absorptive ion transport in distal colons of mice that lack ClC-2 channels."xsd:string
http://purl.uniprot.org/citations/22079595http://purl.uniprot.org/core/volume"142"xsd:string
http://purl.uniprot.org/citations/22079595http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/22079595
http://purl.uniprot.org/citations/22079595http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/22079595
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