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Role for p27(Kip1) in Vascular Smooth Muscle Cell Migration

J Sun1, S O Marx, H J Chen

  • 1Cardiology Division, Center for Molecular Cardiology, Department of Medicine, Columbia University College of Physicians and Surgeons, Mount Sinai School of Medicine, New York, NY, USA.

Circulation
|June 20, 2001
PubMed
Abstract

Insights

The cyclin-dependent kinase inhibitor p27(Kip1) is crucial for rapamycin's ability to inhibit smooth muscle cell migration. Its absence significantly reduces rapamycin's antimigratory effects, highlighting its role in regulating cell movement.

Area of Science:

  • Vascular Biology
  • Cell Signaling
  • Pharmacology

Background:

  • Rapamycin inhibits smooth muscle cell (SMC) proliferation and migration.
  • SMC proliferation inhibition by rapamycin involves p27(Kip1) upregulation.
  • p27(Kip1) plays a role in rapamycin's antiproliferative effects.

Purpose of the Study:

  • To investigate the role of p27(Kip1) in mediating the antimigratory effects of rapamycin on SMCs.
  • To determine if p27(Kip1) is essential for rapamycin-induced inhibition of SMC migration.

Main Methods:

  • Assessing rapamycin's effect on basic fibroblast growth factor-induced SMC migration in wild-type (WT) and p27(Kip1)(-/-) cells using a modified Boyden chamber.
  • Evaluating rapamycin's impact on aortic SMC explant migration in WT, p27(+/-), and p27(-/-) mice.

Main Results:

  • Rapamycin dose-dependently inhibited WT SMC migration but not p27(Kip1)(-/-) SMC migration.
  • Systemic rapamycin administration significantly inhibited SMC migration in WT and p27(Kip1)(+/-) mice by 90%.
  • p27(Kip1)(-/-) mice showed no significant inhibition of SMC migration in response to rapamycin.

Conclusions:

  • The absence of p27(Kip1) diminishes the inhibitory effect of rapamycin on SMC migration.
  • p27(Kip1) is implicated in the signaling pathways governing SMC migration.
  • p27(Kip1) is a key mediator of rapamycin's antimigratory action on smooth muscle cells.

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