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C-reactive protein-induced upregulation of extracellular matrix metalloproteinase inducer in macrophages: inhibitory effect of fluvastatin.

机译：C反应蛋白诱导巨噬细胞中细胞外基质金属蛋白酶诱导剂的上调：氟伐他汀的抑制作用。

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OBJECTIVE: Extracellular matrix metalloproteinase inducer (EMMPRIN) and matrix metalloproteinase (MMP)-9 were reported to be expressed at the macrophage-rich area in human coronary atherosclerotic plaque. We examined whether C-reactive protein (CRP) activates macrophages to express EMMPRIN and MMP-9 in vitro and whether statins inhibit it. METHODS AND RESULTS: Rat peritoneal macrophages were collected by peritoneal lavage, and were incubated in the presence or absence of CRP. CRP at 5 microg/ml increased the gene expression of EMMPRIN relative to GAPDH, measured by RT-PCR, by 1.67+/-0.07 fold at 24 h and by 1.85+/-0.49 fold at 48 h (both p<0.05). The gene expression of MMP-9 in the presence of CRP at 5 microg/ml was followed by 1.36+/-0.11 fold increase at 24 h and by 3.95+/-0.81 fold at 48 h (both p<0.05). CRP at 5 microg/ml for 48 h increased by 6 fold MMP-9 activity, measured by zymography, without affecting tissue inhibitor of metalloproteinases-1. Boiled CRP at 5 mug/ml for 48 h unaffected MMP-9 activity. Fluvastatin blocked the CRP-induced increases in EMMPRIN and MMP-9 expression and activity. Diphenylene iodonium, an inhibitor of NADPH oxidase, had a similar effect on MMP-9 activity. Fluvastatin suppressed the CRP-induced increases in 8-epi-prostaglandin F(2alpha) levels in the condition media. CONCLUSIONS: CRP is an activator for macrophages to enhance EMMPRIN and MMP-9 expression. Fluvastatin inhibits them presumably through its antioxidant effect.
机译：目的：据报道细胞外基质金属蛋白酶诱导剂（EMMPRIN）和基质金属蛋白酶（MMP）-9在人冠状动脉粥样斑块中富含巨噬细胞的区域表达。我们检查了C反应蛋白（CRP）是否在体外激活巨噬细胞以表达EMMPRIN和MMP-9，以及他汀类药物是否抑制了它。方法和结果：通过腹膜灌洗收集大鼠腹膜巨噬细胞，并在有或没有CRP的情况下进行培养。通过RT-PCR测定，相对于GAPDH，5 microg / ml的CRP使EMMPRIN的基因表达在24小时增加了1.67 +/- 0.07倍，在48小时增加了1.85 +/- 0.49倍（均p <0.05）。在存在CRP且浓度为5 microg / ml的情况下，MMP-9的基因表达在24小时后增加1.36 +/- 0.11倍，在48小时时增加3.95 +/- 0.81倍（均p <0.05）。通过酶谱法测定，以5微克/毫升持续48小时的CRP增加了6倍的MMP-9活性，而没有影响金属蛋白酶-1的组织抑制剂。以5杯/毫升的水煮沸的CRP，持续48小时不影响MMP-9活性。氟伐他汀阻止了CRP诱导的EMMPRIN和MMP-9表达和活性的增加。 NADPH氧化酶的抑制剂二亚苯基碘鎓对MMP-9活性具有相似的作用。氟伐他汀抑制条件介质中CRP诱导的8-e-前列腺素F（2alpha）水平增加。结论：CRP是巨噬细胞的活化剂，可增强EMMPRIN和MMP-9的表达。氟伐他汀大概通过其抗氧化作用抑制了它们。

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