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Identification of Cyclin-dependent Kinase 1 Specific Phosphorylation Sites by an In Vitro Kinase Assay
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Cyclin-dependent kinase 5 mediates pleiotrophin-induced endothelial cell migration

Evgenia Lampropoulou1, Ioanna Logoviti1, Marina Koutsioumpa1,2

  • 1Laboratory of Molecular Pharmacology, Department of Pharmacy, University of Patras, GR26504, Patras, Greece.

Scientific Reports
|April 14, 2018
PubMed

Insights

Pleiotrophin (PTN) activates cyclin-dependent kinase 5 (CDK5) via receptor RPTPβ/ζ, promoting endothelial cell migration. Inhibiting CDK5 blocks PTN

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Biochemistry

Background:

  • Pleiotrophin (PTN) is a growth factor that stimulates endothelial cell migration.
  • PTN signaling involves receptor protein tyrosine phosphatase beta/zeta (RPTPβ/ζ) and ανβ3 integrin.
  • Cyclin-dependent kinase 5 (CDK5) is implicated in cell migration.

Purpose of the Study:

  • To identify proteins interacting with RPTPβ/ζ and regulating PTN signaling.
  • To investigate the role of CDK5 in PTN-induced endothelial cell migration.
  • To evaluate a novel pyrrolo[2,3-α]carbazole derivative as a potential CDK5 inhibitor.

Main Methods:

  • Mass spectrometry to identify interacting proteins.
  • Protein immunoprecipitation and proximity ligation assays to confirm interactions.
  • Pharmacological and genetic inhibition of CDK5 to assess its role in cell migration.

Main Results:

  • Cyclin-dependent kinase 5 (CDK5) activator p35 was identified as an RPTPβ/ζ interacting protein.
  • PTN activates CDK5 in endothelial cells via RPTPβ/ζ and phosphoinositide 3-kinase (PI3K) signaling.
  • CDK5 inhibition abolished PTN-induced endothelial cell migration.
  • A pyrrolo[2,3-α]carbazole derivative suppressed CDK5 activity and PTN-induced migration.

Conclusions:

  • CDK5 is a key mediator of PTN-induced endothelial cell migration.
  • PTN activates CDK5 through an RPTPβ/ζ-dependent pathway.
  • CDK5 is a potential therapeutic target for inhibiting PTN's pro-angiogenic effects.

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