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Cell-type- and cell-cycle-specific anti-mitogenesis by cicaprost

Paola Castagnino1, Devashish Kothapalli, Elizabeth A Hawthorne

  • 1Department of Pharmacology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104-6084, United States. pcastagn@mail.med.upenn.edu

Prostaglandins & Other Lipid Mediators
|May 12, 2010
PubMed

Insights

Stable PGI(2) mimetics, like cicaprost, show promise as specific inhibitors of vascular smooth muscle cell proliferation. Unlike rapamycin, cicaprost selectively targets VSMCs, potentially reducing angioplasty complications.

Area of Science:

  • Cardiovascular Research
  • Pharmacology
  • Cell Biology

Background:

  • Drug-eluting stents aim to limit restenosis by inhibiting cell proliferation.
  • Current anti-proliferative drugs lack specificity, affecting both intimal endothelial and medial smooth muscle cells, potentially causing complications.
  • A need exists for more specific anti-proliferative agents to improve angioplasty outcomes.

Purpose of the Study:

  • To compare the anti-proliferative effects of rapamycin and cicaprost, a prostacyclin (PGI2) mimetic.
  • To determine the specificity of cicaprost in inhibiting vascular smooth muscle cell (VSMC) proliferation compared to endothelial cells.
  • To investigate the role of p27(kip1) in the anti-mitogenic mechanisms of rapamycin and cicaprost.

Main Methods:

  • Comparative analysis of rapamycin and cicaprost on vascular smooth muscle cells (VSMCs) and aortic endothelial cells.
  • Assessment of mitogenesis inhibition at various drug concentrations.
  • Evaluation of drug effects in p27(kip1)-null VSMCs to elucidate mechanism of action.

Main Results:

  • Both rapamycin and cicaprost demonstrated strong anti-mitogenic effects on VSMCs.
  • Cicaprost did not inhibit endothelial cell mitogenesis, even at supra-therapeutic concentrations for VSMCs.
  • Cicaprost's anti-mitogenic effect was dependent on p27(kip1), whereas rapamycin's effect was not.

Conclusions:

  • Stable PGI2 mimetics, such as cicaprost, are highly specific inhibitors of VSMC proliferation.
  • Cicaprost's specificity is linked to its dependence on p27(kip1).
  • PGI2 mimetics represent a promising therapeutic strategy for selectively inhibiting VSMC proliferation post-vascular injury, potentially improving angioplasty outcomes.

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