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Related Concept Videos

Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
Positive Regulator Molecules02:39

Positive Regulator Molecules

Mitotic cell division results in daughter cells that exactly resemble the parent cell. However, errors in the DNA replication or distribution of genetic material may lead to genetic mutations that may be passed down to every new cell formed from the resulting abnormal cell. Propagation of such mutant cells is restricted through checkpoint mechanisms present at different stages of the cell cycle. These checkpoints involve regulator molecules that either promote or demote cell cycle events.
Positive Regulator Molecules01:45

Positive Regulator Molecules

To consistently produce healthy cells, the cell cycle—the process that generates daughter cells—must be precisely regulated.
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
M-Cdk Drives Transition Into Mitosis02:15

M-Cdk Drives Transition Into Mitosis

Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...

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Related Experiment Video

Updated: Jun 13, 2026

Isolation and Staining of Mouse Skin Keratinocytes for Cell Cycle Specific Analysis of Cellular Protein Expression by Mass Cytometry
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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
Summary

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.

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Last Updated: Jun 13, 2026

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Published on: May 9, 2019

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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.