Atsumi T, Nishihira J, Makita Z, Koike T
Department of Medicine II, Hokkaido University School of Medicine, Sapporo, 060-8638, Japan.
Cytokine. 2000 Oct;12(10):1553-6. doi: 10.1006/cyto.2000.0745.
We examined the expression of macrophage migration inhibitory factor (MIF) mRNA in murine macrophage cell line (RAW 264.7 cells) in response to oxidized low-density lipoprotein (oxLDL), and investigated the influence of MIF on the uptake and degradation of oxLDL by RAW 264.7 cells. MIF mRNA expression was markedly upregulated in the presence of oxLDL. Consistent with this, the MIF level of the culture medium was increased by stimulation with oxLDL in dose- and time-dependent manners. Next, we added recombinant rat MIF to the culture medium and examined its effects on the uptake of(125)I-labelled oxLDL. Pretreatment with MIF enhanced both the uptake and degradation of(125)I-oxLDL. Taken together, these results suggest that MIF released from macrophages in response to oxLDL stimulates oxLDL uptake and degradation in an autocrine and paracrine fashion, which potentially results in atherosclerosis.
我们检测了鼠巨噬细胞系（RAW 264.7细胞）中巨噬细胞移动抑制因子（MIF）mRNA对氧化型低密度脂蛋白（oxLDL）的反应，并研究了MIF对RAW 264.7细胞摄取和降解oxLDL的影响。在oxLDL存在的情况下，MIF mRNA表达明显上调。与此一致的是，oxLDL刺激使培养基中的MIF水平呈剂量和时间依赖性增加。接下来，我们将重组大鼠MIF添加到培养基中，并检测其对摄取（125）I标记的oxLDL的影响。用MIF预处理可增强（125）I-oxLDL的摄取和降解。综上所述，这些结果表明，巨噬细胞响应oxLDL释放的MIF以自分泌和旁分泌方式刺激oxLDL的摄取和降解，这可能导致动脉粥样硬化。
