Cordycepin inhibits vascular smooth muscle cell proliferation

Woochul Chang1, Soyeon Lim, Heesang Song

  • 1Cardiovascular Research Institute, Cardiology Division, Department of Internal Medicine, Brain Korea 21 Project for Medical Science, Yonsei University College of Medicine, Seoul, 120-752, South Korea.

Insights

Cordycepin treatment reduced neointimal formation in balloon-injured rat carotid arteries, inhibiting vascular smooth muscle cell proliferation. This suggests cordycepin may be a potential therapeutic for restenosis by modulating vessel wall remodeling.

Area of Science:

  • Cardiovascular Biology
  • Pharmacology
  • Cell Biology

Background:

  • Percutaneous transluminal coronary angioplasty (PTCA) is limited by restenosis, a process involving vascular remodeling and extracellular matrix accumulation.
  • The matrix metalloproteinase (MMP) system is implicated in restenosis and atherosclerosis.
  • Cordycepin exhibits various pharmacological activities, but its effect on restenosis is unclear.

Purpose of the Study:

  • To investigate the therapeutic potential of cordycepin in preventing restenosis.
  • To elucidate the mechanism of cordycepin's action on the MMP system in vascular smooth muscle cells.

Main Methods:

  • Balloon injury model in Sprague-Dawley rat carotid arteries.
  • Treatment with cordycepin (20 microM/day, i.p.).
  • Assessment of neointimal formation, rat aortic smooth muscle cell (RaoSMC) proliferation, MMP-2 and -9 activation, extracellular matrix metalloproteinase inducer (EMMPRIN) expression, and cyclooxygenase-2 (COX-2) expression in collagen type I-activated RaoSMCs.

Main Results:

  • Cordycepin treatment reduced neointimal formation in balloon-injured rat carotid arteries.
  • Cordycepin inhibited RaoSMC proliferation.
  • Cordycepin dose-dependently inhibited MMP-2 and -9 activation and EMMPRIN expression in activated RaoSMCs.
  • Cordycepin suppressed COX-2 expression.

Conclusions:

  • Cordycepin demonstrates antiproliferative effects on RaoSMCs, likely through modulation of vessel wall remodeling.
  • Cordycepin's inhibition of MMP activation and EMMPRIN expression suggests a role in preventing restenosis.
  • Cordycepin represents a potential therapeutic strategy for treating restenosis and atherosclerosis.

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