• Tenascin-X induces cell detachment through p38 mitogen-activated protein kinase activation.

Fujie, Shinpei

Maita, Hiroshi

Ariga, Hiroyoshi

Matsumoto, Ken-ichi

  • NDC 499
  • MeSH Animals
  • MeSH Cell Adhesion/physiology
  • MeSH Cells, Cultured
  • MeSH Extracellular Matrix Proteins/metabolism
  • MeSH Fibroblasts/metabolism
  • MeSH Focal Adhesion Protein-Tyrosine Kinases/metabolism
  • MeSH Mice
  • MeSH Phosphorylation
  • MeSH Signal Transduction
  • MeSH Tenascin/metabolism
  • MeSH p38 Mitogen-Activated Protein Kinases/metabolism
  • Extracellular matrix glycoprotein tenascin-X (TNX) is the largest member of the tenascin family. In this study, we investigated the adhesive properties of TNX and the signaling pathway to be induced to mouse fibroblast L cells on TNX substrate. Approximately 45% of evaluable cells used in the cell adhesion assay were attached to purified TNX but did not spread and were rounded on TNX. The remaining 55% of cells were detached from the TNX substrate and were floating in the conditioned medium. In rounded cells on TNX, phosphorylation of focal adhesion kinase (FAK) was diminished compared with that in cells on control phosphate buffered saline (PBS). To better understand the pathways that lead to the detachment of cells on the TNX substrate, we examined phosphorylation of p38 mitogen-activated protein (MAP) kinase. Phosphorylation of p38 MAP kinase was observed in the rounded cells on TNX in a dose-dependent manner, and the maximum effect was observed at 30 min on TNX. Inhibition of p38 MAP kinase alpha expression by RNA interference partially suppressed the TNX-induced cell detachment. These results suggest that the p38 MAP kinase is a major mediator of TNX-induced cell detachment.
PublisherThe Pharmaceutical Society of Japan
Date Issued 2009-10
NIItypejournal article
Identifier URI
  • isIdenticalTo PMID 19801846
  • isIdenticalTo DOI
    • ISSN 1347-5215
    • Biological & pharmaceutical bulletin
    32(10), 1795-1799