Journal
CELL BIOLOGY INTERNATIONAL
Volume 43, Issue 1, Pages 73-82Publisher
WILEY
DOI: 10.1002/cbin.11074
Keywords
claudins; diabetic nephropathy; mannitol; MDCK cells; osmolality; paracellular epithelial barrier
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Funding
- Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq, Brazil) [304991/2015-5]
- CNPq (Brazil)
- FAEPEX-UNICAMP [2048/15]
- FAPESP, Brazil [2013/15676-0]
- Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP) [13/15676-0] Funding Source: FAPESP
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Osmotic alterations are associated with several human diseases, including diabetic nephropathy. We have previously shown that high glucose, which is a well-known osmotic agent, induces significant disruption of the tight junction (TJ)-mediated tubular barrier of the Madin-Darby canine kidney (MDCK) cell line. In this study, we investigated the effect of acute (24 h) and chronic (72 h) exposure to increased osmolality (with a 14.5 mM mannitol solution) on TJ-mediated barrier function in MDCK cells. The treatment with mannitol significantly increased the transepithelial electrical resistance (TEER) and accelerated the TEER recovery after Ca2+ switch assay in comparison with control monolayers. Immunofluorescence and Western blot analyses showed that mannitol treatment induced a significant increase in the tight junctional and cellular content of claudin-1 (a barrier-forming claudin) as well as a significant decrease in claudin-2 (a pore-forming claudin) junctional and cellular contents. These data suggest that an increased osmolality induces enhancement of the TJ-mediated barrier of MDCK cells, and that, therefore, the negative effect of high glucose on the epithelial paracellular barrier cannot be attributed to its osmotic actions. In addition, a subtle increase in osmolality may have an impact on kidney function and renal-related diseases.
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