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1 Veterinary Biomedical Sciences, University of Saskatchewan, Saskatoon, SK, Canada
2 Small Animal Clinical Sciences, University of Saskatchewan, Saskatoon, SK, Canada
* To whom correspondence should be addressed. E-mail: george.forsyth{at}usask.ca.
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 chloride transporters involved in basal fluid transfer across the RPE have been compared to determine whether calcium-dependent or cAMP-dependent channels may be responsible for basal housekeeping levels of secretory activity in this tissue. The role of a candidate calcium-dependent CLCA protein in the basal RPE transport of chloride has been investigated. Low concentrations of the chloride 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 calcium-dependent chloride efflux from fibroblasts expressing the pCLCA1 chloride conductance regulator. However, these same agents did not inhibit the rate of chloride release from cultured fibroblasts expressing the cystic fibrosis transmembrane regulator (CFTR) conductive chloride 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 chloride ion from both types of cultured cells. However, the presence of pCLCA1 also increased cAMP-dependent chloride ion release from fibroblasts expressing CFTR. We conclude that Ca2+-dependent chloride transport may be more important than cAMP-dependent chloride transport for normal fluid secretion across the RPE. Further, it appears that CLCA proteins expressed in the RPE may regulate the activity of other chloride transporters, rather than functioning as primary ion transport proteins.
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