期刊
JOURNAL OF CELLULAR PHYSIOLOGY
卷 226, 期 6, 页码 1471-1478出版社
WILEY-BLACKWELL
DOI: 10.1002/jcp.22386
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资金
- KAKENHI [20790175]
- Ministry of Education, Science, Sports, and Culture of Japan
- Salt Science Research Foundation [0830]
- Mochida Memorial Foundation for Medical and Pharmaceutical Research
- Mishima Kaiun Memorial Foundation
- SRI academic research grant
- Grants-in-Aid for Scientific Research [21590170, 20790175] Funding Source: KAKEN
Migration of renal epithelial cells increases after renal tubular damage, but its mechanism has not been clarified in detail. Hyperosmotic stress increased a cellular injury concomitant with a decrease in mRNA and protein expression of claudin-2 in renal tubular epithelial Madin-Darby canine kidney cells. We hypothesized that claudin-2 is involved in the regulation of cell migration. To knockdown claudin-2 expression, we made the cells expressing doxycycline-inducible claudin-2 shRNA vector. Claudin-2 knockdown affected neither the endogenous expression levels of claudin-1, -3, -4, and -7 nor the Triton X-100 solubility of these claudins. Transepithelial electrical resistance was increased by claudin-2 knockdown without affecting permeability to FITC-dextran (4,000 Da). BrdU incorporation assay and cell counting revealed that cell proliferation and viability are unaffected by claudin-2 knockdown. In the wound-healing assay, the recovery rate of wound area was increased by claudin-2 knockdown. The mRNA expression and activity of matrix metalloproteinase-9 (MMP-9) were increased by claudin-2 knockdown. A selective MMP-9 inhibitor suppressed cell migration in the claudin-2 knockdown cells. Hyperosmotic stress increased the expression and activity of MMP-9, which were inhibited by claudin-2 overexpression. These results suggest that the decrease in claudin-2 expression enhances cell migration mediated by the increase in the expression and activity of MMP-9. J. Cell. Physiol. 226: 1471-1478, 2011. (C) 2010 Wiley-Liss, Inc.
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