Enhancement of cell–cell contact by claudin-4 in renal epithelial madin-darby canine kidney cells

✍ Scribed by Akira Ikari; Kosuke Atomi; Ayumi Takiguchi; Yasuhiro Yamazaki; Hisayoshi Hayashi; Jotaro Hirakawa; Junko Sugatani

• Publisher: John Wiley and Sons
• Year: 2012
• Tongue: English
• Weight: 828 KB
• Volume: 113
• Category: Article
• ISSN: 0730-2312
• DOI: 10.1002/jcb.23373

✦ Synopsis

Abstract

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 cell–cell contact in renal tubular epithelial cells. J. Cell. Biochem. 113: 499–507, 2012. © 2011 Wiley Periodicals, Inc.