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This Article Full Text Full Text (PDF) All Versions of this Article: 285/5/C1314    most recent 00210.2003v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (18) Citing Articles via Google Scholar Google Scholar Articles by Loewen, M. E. Articles by Forsyth, G. W. Search for Related Content PubMed PubMed Citation Articles by Loewen, M. E. Articles by Forsyth, G. W.

MEMBRANE TRANSPORTERS, ION CHANNELS, AND PUMPS

CLCA protein and chloride transport in canine retinal pigment epithelium

Departments of ¹Veterinary Biomedical Sciences and ²Small Animal Clinical Sciences, Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada S7N 5B4

Submitted 20 May 2003 ; accepted in final form 8 July 2003

Problems in ion and fluid transfer across the retinal pigment epithelium (RPE) are a probable cause of inappropriate accumulations of fluid between the photoreceptors of the retina and the RPE. The activities of Cl^- transporters involved in basal fluid transfer across the RPE have been compared to determine whether Ca²⁺- or cAMP-dependent channels may be responsible for basal housekeeping levels of secretory activity in this tissue. The role of a candidate Ca²⁺-dependent CLCA protein in the basal RPE transport of Cl^- has been investigated. Low concentrations of the Cl^- conductance inhibitors glibenclamide and 5-nitro-2-(3-phenylpropylamino)benzoate reduced the short-circuit current in dog RPE preparations mounted in Ussing chambers and decreased the Ca²⁺-dependent Cl^- efflux from fibroblasts expressing the pCLCA1 Cl^- conductance regulator. However, these same agents did not inhibit the rate of Cl^- release from cultured fibroblasts expressing the cystic fibrosis transmembrane regulator (CFTR) conductive Cl^- channel. Addition of ionomycin to primary cultures of canine RPE cells or to fibroblasts expressing the pCLCA1 channel regulator increased the rate of release of Cl^- from both types of cultured cells. However, the presence of pCLCA1 also increased cAMP-dependent Cl^- release from fibroblasts expressing CFTR. We conclude that Ca²⁺-dependent Cl^- transport may be more important than cAMP-dependent Cl^- transport for normal fluid secretion across the RPE. Furthermore, CLCA proteins expressed in the RPE appear to regulate the activity of other Cl^- transporters, rather than functioning as primary ion transport proteins.

chloride channel; cystic fibrosis transmembrane conductance regulator, calcium; fluid secretion

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