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Updated: Jul 20, 2026

Murine Aortic Crush Injury: An Efficient In Vivo Model of Smooth Muscle Cell Proliferation and Endothelial Function
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Intracellular signaling pathways required for rat vascular smooth muscle cell migration. Interactions between basic

C Bilato1, R R Pauly, G Melillo

  • 1Laboratory of Cardiovascular Science, National Institute on Aging, National Institutes of Health, Baltimore, Maryland 21224, USA.

The Journal of Clinical Investigation
|October 1, 1995
PubMed

Insights

Basic fibroblast growth factor (bFGF) is essential for platelet-derived growth factor (PDGF)-driven vascular smooth muscle cell (VSMC) migration. bFGF links PDGF signaling to calcium transients and CamKinase II activation, crucial for VSMC migration.

Area of Science:

  • Vascular Biology
  • Cell Signaling
  • Molecular Medicine

Background:

  • Vascular smooth muscle cell (VSMC) migration is critical in vascular disease pathogenesis.
  • Platelet-derived growth factor (PDGF) and basic fibroblast growth factor (bFGF) activate intracellular pathways influencing VSMC migration.

Purpose of the Study:

  • To elucidate the role of bFGF in PDGF-directed VSMC migration.
  • To investigate the involvement of calcium signaling and CamKinase II in this process.

Main Methods:

  • Utilized neutralizing antibodies against bFGF.
  • Assessed intracellular calcium transients and CamKinase II activation.
  • Employed ionomycin and site-directed mutagenesis to manipulate calcium levels and CamKinase II activity.

Main Results:

  • bFGF, though a weak chemoattractant itself, is required for PDGF-induced VSMC migration.
  • Neutralizing bFGF significantly reduced PDGF-stimulated calcium transients, VSMC migration, and CamKinase II activation.
  • Restoring calcium transients or constitutively activating CamKinase II rescued migration and signaling.

Conclusions:

  • bFGF acts as a crucial link between PDGF receptor stimulation and downstream calcium/CamKinase II signaling.
  • CamKinase II plays a central regulatory role in controlling VSMC migration in response to PDGF and bFGF.

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