Inami Norihito, Nomura Shosaku, Shimazu Takayuki, Manabe Kenichi, Kimura Yutaka, Iwasaka Toshiji
Second Department of Internal Medicine, Kansai Medical University, Moriguchi, Osaka, Japan.
J Thromb Thrombolysis. 2007 Dec;24(3):267-73. doi: 10.1007/s11239-007-0042-8. Epub 2007 May 8.
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.
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.
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.
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.
某些因素在经皮冠状动脉介入治疗（PCI）后再狭窄的发生中起致病作用。我们测量并比较了PCI后单核细胞趋化蛋白-1（MCP-1）、正常T细胞激活后表达和分泌的调节蛋白（RANTES）、可溶性（s）P-选择素、sE-选择素和脂联素水平升高的比例。
对96例行PCI且在6个月随访时进行了重复血管造影的患者（69例男性和27例女性，年龄63±9岁），在PCI前和PCI后30天测量血浆趋化因子和可溶性标志物水平。此外，我们开展了MCP-1对单核细胞系（THP-1）组织因子表达的基础研究。
33例（34.4%）患者发生再狭窄。在再狭窄组中观察到MCP-1显著且呈时间依赖性增加。然而，无论有无再狭窄，RANTES、sP-选择素和sE-选择素水平均无显著差异。冠心病患者的脂联素水平显著低于正常对照组。然而，有无再狭窄的患者在基线时脂联素水平并无差异。MCP-1未诱导THP-1上组织因子的表达。然而，添加MCP-1可增强重组sCD40配体诱导的THP-1上组织因子的表达。
这些发现提示，冠心病患者PCI后再狭窄的发生可能涉及PCI后MCP-1的参与，且脂联素不能完全预防这种依赖MCP-1的再狭窄。
