Inhibition of extracellular signal-regulated kinase downregulates claudin-2 expression and alters paracellular permeability in mouse rectum CMT93-II cells

Tetsuichiro Inai, Norio Kitagawa, Yuji Hatakeyama, Tetsuro Ikebe, Hiroshi Iida, Mamoru Fujita

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

The morphological and physiological properties of tight junctions (TJs) are determined by the combination and mixing ratios of claudin species. Mouse rectum carcinoma cell lines, CMT93-I and -II cells, expressed claudin-4, -6, -7, and -12, and CMT93-II cells further expressed claudin-2. Although there were no differences in the morphology and number of TJ strands between the two cell lines, transepithelial electrical resistance (TER) of CMT93-II cells was approximately one-seventh that of CMT93-I cells. In this study, we aimed to determine whether claudin-2 expression in CMT93-II cells caused the reduction of TER. Inhibition of the extracellular signal-regulated kinase (ERK) pathway by U0126 treatment for 24 and 48. h in CMT93-II cells markedly decreased claudin-2 from the apical junctional region and increased TER. However, claudin-4, -6, and -7 were still continuously localized at the apical junctional region by U0126 treatment. Moreover, the claudin-2 expression recovered at the apical junctional region after the removal of U0126 and TER decreased almost to the baseline level. These results suggest that the ERK pathway positively regulates claudin-2 protein expression and claudin-2 is involved in lowering TER in CMT93-II cells.

Original languageEnglish
Pages (from-to)175-182
Number of pages8
JournalTissue and Cell
Volume45
Issue number3
DOIs
Publication statusPublished - Jun 2013

    Fingerprint

All Science Journal Classification (ASJC) codes

  • Developmental Biology
  • Cell Biology

Cite this