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Murine Aortic Crush Injury: An Efficient In Vivo Model of Smooth Muscle Cell Proliferation and Endothelial Function
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Mitogen crosstalk accompanying urokinase receptor expression in stimulated vascular smooth muscle cells

U Reuning1, E P Dixon, S P Little

  • 1Frauenklinik der Technischen Universität München, Germany.

FEBS Letters
|August 26, 1996
PubMed

Insights

Mitogens like thrombin and bFGF regulate urokinase-type plasminogen activator receptor (uPAR) mRNA in smooth muscle cells. Interactions reveal complex feedback, influencing uPAR expression through autoinduction and receptor regulation.

Area of Science:

  • Vascular Biology
  • Cell Signaling
  • Molecular Biology

Background:

  • Urokinase-type plasminogen activator receptor (uPAR) expression is modulated by mitogens in vascular smooth muscle cells (SMC).
  • Understanding the interplay between different mitogens is crucial for elucidating uPAR regulation.

Purpose of the Study:

  • To investigate the interactions between mitogens that influence uPAR mRNA levels in bovine SMC.
  • To identify feedback mechanisms regulating uPAR mRNA expression.

Main Methods:

  • Quantitative analysis of mRNA levels for uPAR, bFGF, bFGF-R, and TGF-beta1 in response to mitogen stimulation.
  • Utilized bovine aorta SMC models.

Main Results:

  • Thrombin and bFGF up-regulated uPAR mRNA, preceded by increased bFGF mRNA. PDGF increased uPAR mRNA but decreased bFGF mRNA.
  • Both thrombin and bFGF induced bFGF receptor (bFGF-R) mRNA. Thrombin also increased TGF-beta1 mRNA.
  • Demonstrated both positive and negative feedback loops between mitogens at the mRNA level.

Conclusions:

  • Complex feedback mechanisms, including autoinduction and receptor regulation by bFGF, contribute to fine-tuning uPAR mRNA levels.
  • Cooperation and amplification of mitogenic signals likely play a role in uPAR mRNA regulation in stimulated SMC.

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