小鼠血管损伤后巨噬细胞与平滑肌细胞的相互作用

Interaction between Macrophages and Smooth Muscle Cells in Lesion Formation after Vascular Injury in Mice

目的研究血管损伤后病变形成过程中的巨噬细胞与平滑肌细胞的相互作用。方法C57BL/6(6～8周龄)小鼠24只,右侧股动脉植入透明塑料微导管,制作小鼠血管损伤模型,术后给予特异性抗体AFS98及APB5,分别阻断巨噬细胞和平滑肌细胞增殖的信息传导通路。给药2周后采集股动脉组织,用免疫组织化学的方法对血管病变进行分析。结果小鼠股动脉血管损伤2周后,病变部位聚集了大量的巨噬细胞、平滑肌细胞。给予阻断巨噬细胞增殖的信息传导通路的特异性抗体AFS98后,病变部位的巨噬细胞数量显著减少,平滑肌细胞数量反而增多。相反,给予抑制平滑肌细胞增殖的抗体APB5后,病变局部平滑肌细胞数量减少,而巨噬细胞数量急剧增加。结论小鼠股动脉血管损伤后,构成病变的细胞主要为巨噬细胞与平滑肌细胞。这两种细胞在分化成终末成熟细胞的过程中,存在着相互拮抗的作用。

Objective To study the regulatory roles of macrophages and smooth muscle cells in lesion formation induced by polyethylene cuff placement. Methods C57BL/6 mice （8 - 10 weeks of age） were used to establish vascular injury model. A noneonstrietive cuff was placed around the fight femoral artery. To block the receptor tyrosine kinase signal pathway, monoclonal antibody AFS98 against macrophage-colony stimulating factor receptor c-fins or antibody APB5 against platelet-derived growth factor reeeptor-β was administered. After another 2 weeks, both right and left femoral arteries were taken and subjected to histochemical analysis. Results In the mice that had not received either antibody, a large number of macrophages and smooth muscle cells were detected in the right femoral artery, whereas such cells was not observed in the sham-operated left artery. In the right artery from the mice given AFS98, the cell density recognized by anti-macrophage antibody BM8 was markedly reduced. In striking contrast, the mice given APB5 showed an increase in the number of maerophages and a relative decrease in SMC density in the right artery. Conclusion There are numerous maerophages and smooth muscle cells aggregated in the femoral artery injuried by cuff placement in mice. Maerophages and smooth muscle cells may play opposite roles in the lesion formation.