Related Experiment Video
Updated: Jul 1, 2026

Isolation of Primary Patient-specific Aortic Smooth Muscle Cells and Semiquantitative Real-time Contraction Measurements In Vitro
Published on: February 15, 2022
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.
Abstract:
Percutaneous transluminal coronary angioplasty (PTCA) is a common procedure for treating atherosclerosis, but its efficacy is limited because of the occurrence of restenosis within 3-6 months after angioplasty. Restenosis is induced by the remodeling of the vessel wall and/or the accumulation of cells and extracellular matrix (ECM) in the intimal layer. Therefore, the matrix metalloproteinase (MMP) system may be a potential therapeutic target for the treatment of restenosis or atherosclerosis. Cordycepin is reported to possess many pharmacological activities including immunological stimulating, anti-cancer, antioxidant, and anti-inflammatory activities. The effect of cordycepin on restenosis has not yet been clearly elucidated. Therefore, in the present study, we tested the role of cordycepin on the MMP system in vascular smooth muscle cells. In the carotid artery of a balloon-injured Sprague-Dawley (SD) rat, neointimal formation was reduced by treatment with cordycepin (20 microM/day, i.p), which inhibited the proliferation of rat aortic smooth muscle cells (RaoSMCs). To investigate the mechanism by which cordycepin inhibits the remodeling of the vessel wall and/or the accumulation of cells and ECM, we examined the activation of MMP systems in collagen type I-activated RaoSMCs. Cordycepin markedly inhibited the activation of MMP-2 and -9 as well as the expression of extracellular matrix metalloproteinase inducer (EMMPRIN) in a dose-dependent manner in collagen type I-activated RaoSMCs. Moreover, cordycepin suppressed cycloxygenase-2 (COX-2) expression related to hyperplasia of RAoSMCs. Taken together, these data suggest that cordycepin may induce antiproliferation in RAoSMCs via the modulation of vessel wall remodeling. Therefore, cordycepin may be a potential therapeutic approach to treat restenosis.
Related Concept Videos
Antihypertensive Drugs: Action of Calcium Channel Blockers
Inhibition of Cdk Activity
Inhibition of CDK Activity
Smooth Muscle Contraction
The onset of contraction is triggered by an increase in calcium ions within the sarcoplasm, similar to the process in striated muscle. However, smooth muscles have a relatively smaller reservoir of the sarcoplasmic...
Inhibitors of Bacterial Protein Synthesis
Inhibitors of Gram-positive Cell Wall Synthesis

