Journal
JOURNAL OF CELLULAR BIOCHEMISTRY
Volume 113, Issue 2, Pages 499-507Publisher
WILEY-BLACKWELL
DOI: 10.1002/jcb.23373
Keywords
CLAUDIN-4; KIDNEY; CELL-CELL CONTACT; MIGRATION
Categories
Funding
- Research Foundation for Pharmaceutical Sciences (KAKENHI) [23590263]
- SRI Academic Research
- KAKENHI from the Research Foundation for Pharmaceutical Sciences [23590263]
- Grants-in-Aid for Scientific Research [22590068, 23590263] Funding Source: KAKEN
Ask authors/readers for more resources
Claudin-4 regulates ion permeability via a paracellular pathway in renal epithelial cells, but its other physiological functions have not been examined. We found that hyperosmotic stress increases claudin-4 expression in Madin-Darby canine kidney cells. Here, we examined whether claudin-4 affects cell motility, cell association, and the intracellular distribution of endogenous junctional proteins. Doxycycline-inducible expression of claudin-4 did not change endogenous levels of claudin-1, claudin-2, claudin-3, occludin, E-cadherin, and ZO-1. Claudin-4 overexpression increased cell association and decreased cell migration without affecting cell proliferation. Doxycycline did not change cell junctional protein levels, cell association or cell migration in mock-transfected cells. The insolubility of claudin-1 and -3 in Triton X-100 was increased by claudin-4 overexpression, but that of claudin-2, occludin, ZO-1, and E-cadherin was unchanged. Immunocytochemistry showed that claudin-4 overexpression increases the accumulation of claudin-1 and -3 in tight junctions (TJs). Furthermore, claudin-4 overexpression increased the association of claudin-4 with claudin-1 and -3. These results suggest that claudin-4 accumulates claudin-1 and -3 in TJs to enhance cellcell contact in renal tubular epithelial cells. J. Cell. Biochem. 113: 499507, 2012. (C) 2011 Wiley Periodicals, Inc.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available