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Related Experiment Videos

Rac regulates vascular endothelial growth factor stimulated motility.

N Soga1, J O Connolly, M Chellaiah

  • 1Renal Division, Barnes-Jewish Hospital North, Washington University School of Medicine, St. Louis, Missouri 63110, USA.

Cell Communication & Adhesion
|January 5, 2002
PubMed
Summary
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Vascular endothelial growth factor (VEGF) drives endothelial cell migration via Rac activation, crucial for angiogenesis and cancer therapy. Osteopontin-mediated migration bypasses this Rac-dependent pathway.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cancer Research

Background:

  • Endothelial cell migration is vital for angiogenesis, a process targeted in cancer therapy.
  • Vascular endothelial growth factor (VEGF) is a key stimulus for endothelial cell migration.
  • The precise role of rho family GTPases, like Rac, in VEGF-mediated endothelial cell signaling remains unclear.

Purpose of the Study:

  • To elucidate the mechanisms of endothelial cell migration regulated by VEGF and rho GTPases.
  • To investigate the involvement of Rac in VEGF-stimulated endothelial cell chemotaxis and haptotaxis.
  • To differentiate Rac-dependent and Rac-independent pathways of endothelial cell motility.

Main Methods:

  • Utilized a mouse brain endothelial cell line (bEND3) with inducible expression of Rac mutants (V12Rac and N17Rac).

Related Experiment Videos

  • Assessed endothelial cell haptotaxis on substrates coated with collagen, vitronectin, and osteopontin.
  • Investigated the effects of VEGF stimulation on cell migration, actin organization, and stress fiber formation.

    • Main Results:

    • Constitutively active V12Rac enhanced endothelial cell haptotaxis on collagen and vitronectin, further stimulated by VEGF.
    • Osteopontin strongly stimulated haptotaxis independently of VEGF, suggesting a Rac-independent pathway.
    • Inhibition of Rac (N17Rac) blocked VEGF-stimulated chemotaxis and associated cytoskeletal rearrangements.

    Conclusions:

    • Endothelial cell migration is regulated by at least two distinct pathways: one Rac-dependent (matrix/integrin-stimulated) and another Rac-independent (osteopontin-stimulated).
    • VEGF-induced chemotaxis critically relies on Rac activation.
    • Osteopontin-mediated motility may inhibit the Rac pathway, explaining the lack of additive effects with VEGF.