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• W2052555925 abstract "Claudin-7, a member of the claudin family, is highly expressed in distal nephrons of kidneys and has been reported to be involved in the regulation of paracellular Cl − permeability in cell cultures. To investigate the role of claudin-7 in vivo, we generated claudin-7 knockout mice (Cln7 −/− ) by the gene-targeting deletion method. Here we report that Cln7 −/− mice were born viable, but died within 12 days after birth. Cln7 −/− mice showed severe salt wasting, chronic dehydration, and growth retardation. We found that urine Na + , Cl − , and K + were significantly increased in Cln7 −/− mice compared with that of Cln7 +/+ mice. Blood urea nitrogen and hematocrit were also significantly higher in Cln7 −/− mice. The wrinkled skin was evident when Cln7 −/− mice were ∼1 wk old, indicating that they suffered from chronic fluid loss. Transepidermal water loss measurements showed no difference between Cln7 +/+ and Cln7 −/− skin, suggesting that there was no transepidermal water barrier defect in Cln7 −/− mice. Claudin-7 deletion resulted in the dramatic increase of aldosterone synthase mRNA level as early as 2 days after birth. The significant increases of epithelial Na + channel α, Na + -Cl − cotransporter, and aquaporin 2 mRNA levels revealed a compensatory response to the loss of electrolytes and fluid in Cln7 −/− mice. Na + -K + -ATPase α 1 expression level was also greatly increased in distal convoluted tubules and collecting ducts where claudin-7 is normally expressed. Our study demonstrates that claudin-7 is essential for NaCl homeostasis in distal nephrons, and the paracellular ion transport pathway plays indispensable roles in keeping ionic balance in kidneys." @default.
• W2052555925 created "2016-06-24" @default.
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• W2052555925 date "2010-01-01" @default.
• W2052555925 modified "2023-10-15" @default.
• W2052555925 title "Renal salt wasting and chronic dehydration in claudin-7-deficient mice" @default.
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• W2052555925 doi "https://doi.org/10.1152/ajprenal.00450.2009" @default.
• W2052555925 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2806124" @default.
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