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Updated: Jul 15, 2026
A Murine Model of Stent Implantation in the Carotid Artery for the Study of Restenosis
Published on: May 14, 2013
Adiponectin incompletely prevent MCP-1-dependent restenosis after percutaneous coronary intervention [corrected] in
Norihito Inami1, Shosaku Nomura, Takayuki Shimazu
1Second Department of Internal Medicine, Kansai Medical University, Moriguchi, Osaka, Japan.
Background:
Some factors play pathogenic roles in the development of restenosis after percutaneous coronary intervention (PCI). We measured and compared the ratio of elevated levels of monocytic chemotactic peptide-1 (MCP-1), regulated on activation normally T-cell expressed and secreted (RANTES), soluble (s) P-selectin, sE-selectin and adiponectin after PCI.
Methods:
Plasma levels of chemokines and soluble markers were measured before and 30 days after PCI in 96 patients (69 males and 27 females, aged 63 +/- 9 years) who underwent PCI and who had repeated angiograms at a 6-month follow-up. In addition, we carried out the basic study of the tissue factor expression on monocytic cell line (THP-1) by MCP-1.
Results:
Restenosis occurred in 33 (34.4%) patients. A significant and time-dependent increase in MCP-1 was observed in the restenosis group. However, there were no significant differences in RANTES, sP-selectin, and sE-selectin levels with or without restenosis. Adiponectin levels in patients with coronary artery disease were significantly lower than levels in normal controls. However, adiponectin levels were no different at baseline between patients with or without restenosis. MCP-1 did not induce the expression of tissue factor on THP-1. However, the recombinant sCD40 ligand-induced expression of tissue factor on THP-1 was enhanced by the addition of MCP-1.
Conclusion:
These findings suggest that restenosis development after PCI in patients with coronary artery disease may involve the participation of MCP-1 after PCI, and adiponectin incompletely prevent this MCP-1-dependent restenosis.
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