Rac, PAK and p38 regulate cell contact-dependent nuclear translocation of myocardin-related transcription factor

Attila Sebe, András Masszi, Matthew Zulys, Tony Yeung, Pam Speight, Ori D. Rotstein, Hiroyasu Nakano, István Mucsi, Katalin Szászi, András Kapus

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42 Citations (Scopus)

Abstract

We investigated the mechanism whereby cell contact injury stimulates the α-smooth muscle actin (SMA) promoter, a key process for epithelial-mesenchymal transition (EMT) during organ fibrosis. Contact disruption by low-Ca2+ medium (LCM) activated Rac, PAK and p38 MAPK, and triggered the nuclear accumulation of myocardin-related transcription factor (MRTF), an inducer of the SMA promoter. Dominant negative (DN) Rac, DN-PAK, DN-p38, or the p38 inhibitor SB203580 suppressed the LCM-induced nuclear accumulation of MRTF and the activation of the SMA promoter. These studies define novel pathway(s) involving Rac, PAK, and p38 in the regulation of MRTF and the contact-dependent induction of EMT.

Original languageEnglish
Pages (from-to)291-298
Number of pages8
JournalFEBS letters
Volume582
Issue number2
DOIs
Publication statusPublished - Jan 23 2008

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Keywords

  • Cell adhesion
  • Epithelial injury
  • Epithelial-mesenchymal transition
  • MRTF

ASJC Scopus subject areas

  • Biophysics
  • Structural Biology
  • Biochemistry
  • Molecular Biology
  • Genetics
  • Cell Biology

Cite this

Sebe, A., Masszi, A., Zulys, M., Yeung, T., Speight, P., Rotstein, O. D., Nakano, H., Mucsi, I., Szászi, K., & Kapus, A. (2008). Rac, PAK and p38 regulate cell contact-dependent nuclear translocation of myocardin-related transcription factor. FEBS letters, 582(2), 291-298. https://doi.org/10.1016/j.febslet.2007.12.021