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FAK phosphorylation plays a central role in thrombin-induced RPE cell migration.

E D Aguilar-Solis1, I Lee-Rivera1, A Álvarez-Arce1

  • 1Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Mexico City, Mexico.

Cellular Signalling
|April 27, 2017
PubMed
Summary
This summary is machine-generated.

Thrombin triggers retinal pigment epithelial (RPE) cell migration via Focal Adhesion Kinase (FAK) phosphorylation, a key process in proliferative vitreoretinopathy (PVR). Targeting FAK phosphorylation offers a potential strategy for PVR treatment.

Keywords:
Focal adhesionProliferative vitreoretinopathyRetinaSignal transduction

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Area of Science:

  • Ophthalmology
  • Cell Biology
  • Molecular Medicine

Background:

  • Retinal pigment epithelial (RPE) cell migration is crucial in pathologic conditions like proliferative vitreoretinopathy (PVR).
  • Blood-retina barrier (BRB) disruption allows thrombin interaction with RPE cells, promoting migration.
  • Molecular mechanisms of thrombin-induced RPE migration, particularly Focal Adhesion Kinase (FAK) involvement, remain unclear.

Purpose of the Study:

  • Identify thrombin-activated signaling pathways leading to FAK phosphorylation.
  • Determine FAK's role in thrombin-induced RPE cell migration.

Main Methods:

  • Investigated thrombin activation of PAR1 receptors on RPE cells.
  • Utilized biochemical assays to assess FAK autophosphorylation and activation loop phosphorylation.
  • Employed pathway inhibitors (c/nPKC, PI3K/PKC-ζ, Rho/ROCK) to dissect signaling cascades.
  • Monitored focal adhesion disassembly, actin stress fiber formation, and RPE cell migration.

Main Results:

  • Thrombin activation of PAR1 induced FAK autophosphorylation at Y397 and Y576/577.
  • FAK phosphorylation was dependent on c/nPKC, PI3K/PKC-ζ, and Rho/ROCK signaling pathways.
  • Inhibition of these pathways blocked thrombin-induced FAK phosphorylation, focal adhesion disassembly, and RPE cell migration.
  • FAK phosphorylation was essential for thrombin-induced actin stress fiber formation and migration.

Conclusions:

  • Thrombin-induced RPE cell migration and transformation are regulated by FAK tyrosine phosphorylation.
  • FAK signaling pathways are critical mediators of thrombin's effects on RPE cells.
  • Targeting FAK phosphorylation presents a potential therapeutic strategy for PVR.