Source:http://linkedlifedata.com/resource/pubmed/id/20717932
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
2011-3-17
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pubmed:abstractText |
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.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
1097-4652
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pubmed:author | |
pubmed:copyrightInfo |
Copyright © 2010 Wiley-Liss, Inc.
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pubmed:issnType |
Electronic
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pubmed:volume |
226
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1471-8
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pubmed:meshHeading |
pubmed-meshheading:20717932-Animals,
pubmed-meshheading:20717932-Cell Movement,
pubmed-meshheading:20717932-Cell Proliferation,
pubmed-meshheading:20717932-Claudins,
pubmed-meshheading:20717932-Dogs,
pubmed-meshheading:20717932-Electric Impedance,
pubmed-meshheading:20717932-Epithelial Cells,
pubmed-meshheading:20717932-Gene Expression Regulation,
pubmed-meshheading:20717932-Gene Knockdown Techniques,
pubmed-meshheading:20717932-Kidney,
pubmed-meshheading:20717932-Matrix Metalloproteinase 9,
pubmed-meshheading:20717932-Osmotic Pressure,
pubmed-meshheading:20717932-Protease Inhibitors,
pubmed-meshheading:20717932-RNA, Messenger,
pubmed-meshheading:20717932-Tight Junctions
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pubmed:year |
2011
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pubmed:articleTitle |
Decrease in claudin-2 expression enhances cell migration in renal epithelial Madin-Darby canine kidney cells.
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pubmed:affiliation |
Department of Pharmaco-Biochemistry, School of Pharmaceutical Sciences, University of Shizuoka, Shizuoka, Japan. ikari@u-shizuoka-ken.ac.jp
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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