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Altered Expression of Tight Junction Proteins in Cyclosporine Nephrotoxicity

Title
Altered Expression of Tight Junction Proteins in Cyclosporine Nephrotoxicity
Author
김근호
Keywords
Cyclosporine nephrotoxicity; Paracellular permeability; Sodium chloride symporter; Tight junction proteins; WNK4 protein
Issue Date
2011-01
Publisher
KARGER
Citation
AMERICAN JOURNAL OF NEPHROLOGY, v. 33, NO 1, Page. 7-16
Abstract
Background/Aims: The increased permeability of chloride in the distal cortical nephron in cyclosporine nephrotoxicity may involve the transcellular pathway mediated by the thiazide-sensitive Na + -Cl - cotransporter and/or the paracellular pathway mediated by the tight junctions (TJs). Methods: Cyclosporine was subcutaneously administered to Sprague-Dawley rats for 6 (7.5 mg/kg body weight) and 2 (25 mg/kg body weight) weeks, and immunoblot analysis and immunohistochemistry were carried out from the kidneys. Electrically tight epithelial Madin-Darby canine kidney (MDCK) I cells were exposed to cyclosporine for 72 h to measure changes in transepithelial electrical resistance (ΔTER). Results: Cyclosporine treatment induced a decrease in Na + -Cl - cotransporter in rat renal cortex. WNK4 protein was increased in both rat kidneys and MDCK I cells. Occludin was also increased in rat kidneys and MDCK I cells exposed to 100 ng/ml cyclosporine. In contrast, cyclosporine treatment induced a decrease in zonula occludens 1 protein abundance and no changes in claudin-1 and claudin-4 in both rat kidneys and MDCK I cells. As a measure of the barrier to small ions, ΔTER of MDCK monolayers was decreased by 100 ng/ml cyclosporine. Conclusion: Renal TJ proteins are affected by cyclosporine treatment. Changes in TJ protein assembly induced by altered expression of WNK4, occludin, and zonula occludens 1 may affect paracellular permeability.
URI
https://www.karger.com/Article/Abstract/322445
ISSN
0250-8095; 1421-9670
DOI
10.1159/000322445
Appears in Collections:
COLLEGE OF MEDICINE[S](의과대학) > MEDICINE(의학과) > Articles
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