AI Article Synopsis
- The study explores the role of the ClC-2 chloride channel in intestinal ion transport, especially in the context of ClC-2 knockout mice.
- It finds that ClC-2 is mainly expressed in the basolateral membrane of surface cells in the early distal colon (EDC) and is crucial for the electroneutral absorption of sodium (Na+), potassium (K+), and chloride (Cl-) ions.
- Despite lacking ClC-2, the knockout mice show a compensatory increase in a specific type of ion current, suggesting that other pathways may partially compensate for its absence.
Article Abstract
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.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3267842 | PMC |
| http://dx.doi.org/10.1053/j.gastro.2011.10.037 | DOI Listing |
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