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The PI3K-Akt pathway promotes microtubule stabilization in migrating fibroblasts

Keisuke Onishi1, Maiko Higuchi, Tomoko Asakura

  • 1Institute of Molecular and Cellular Biosciences, University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo 113-0032, Japan.

Genes to Cells : Devoted to Molecular & Cellular Mechanisms
|April 3, 2007
PubMed

Insights

Platelet-derived growth factor (PDGF) stabilizes microtubules via the PI3K-Akt pathway. This finding reveals a novel mechanism linking extracellular signals to directed cell migration and cell polarity maintenance.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Directed cell migration is crucial for development and disease.
  • Microtubule stabilization is essential for cell polarity during migration.
  • The regulation of microtubule dynamics by extracellular cues remains incompletely understood.

Purpose of the Study:

  • To investigate the role of the PI3K-Akt signaling pathway in growth factor-mediated microtubule stabilization.
  • To elucidate the mechanism by which extracellular cues regulate microtubule dynamics.

Main Methods:

  • Treatment of NIH 3T3 fibroblasts with platelet-derived growth factor (PDGF).
  • Inhibition of PI3K and Akt signaling pathways using chemical inhibitors and dominant-negative Akt (DN-Akt).
  • Analysis of microtubule stabilization in wounded monolayer cultures.

Main Results:

  • PDGF treatment increased microtubule stabilization in fibroblasts.
  • PI3K inhibition or DN-Akt expression abrogated PDGF-induced microtubule stabilization.
  • Akt activation showed a slight increase in overall microtubule stabilization.
  • Microtubule stabilization in migrating cells was attenuated by PI3K inhibition or DN-Akt.

Conclusions:

  • The PI3K-Akt signaling pathway is pivotal in mediating growth factor-induced microtubule stabilization.
  • Akt regulates microtubule stability, providing a novel link between extracellular cues and directed cell migration.
  • This mechanism is important for establishing and maintaining cell polarity during migration.

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