M-CSF促进RAW 264.7细胞MMP-9的分泌及其可能机制

目的探讨巨噬细胞集落刺激因子(MCSF)致动脉粥样硬化的作用是否与其影响基质金属蛋白酶(MMP)表达和活性改变有关及其可能机制。方法应用明胶酶图分析方法观察MCSF和(或)PD98059对体外培养的RAW264.7细胞MMP9活性的影响;Westerblot检测MCSF和(或)PD98059对体外培养的RAW264.7细胞pERK1/2表达的影响。结果MCSF能增强RAW264.7细胞MMP9的活性,并呈一定的剂量依赖性;同时MCSF也呈时间、浓度依赖性促进pERK1/2的表达;PD98059不仅阻断了ERK1/2的磷酸化,而且也降低了MMP9的活性。结论MCSF可诱导RAW264.7细胞MMP9的活性增加,其机制可能与MCSF激活MAPKERK1/2通路有关。

Wpiegulation of macrophage colony-stimulating factor on protease secretion in RAW 264.7 cell and its possible mechanism

Aim To study the effect of Macrophage colony-stimulating factor(M-CSF) on MMP-9 in RAW 264.7 cell and explore the relationship between atherosclerosis caused by M-CSF and the activity of MMP-9. Methods Gelatin zymography analysis was used to investigate the effect of M-CSF and PD98059 on the activity of MMP-9 in cultured RAW 264.7 cell.Western blot was used to study the effect of M-CSF and PD98059 on the express of p-ERK1/2 in cultured RAW 264.7 cell. Results The enzyme activity of MMP-9 was significantly increased after 24-hour M-CSF treatment.Meanwhile, M-CSF upregulated the expression of p-ERK1/2. Pre-treatment with PD98059 blocked partly the increased expression of p-ERK1/2 and the activity of MMP-9 induced by M-CSF. Conclusion M-CSF can induce the secretion of MMP9 in RAW 264.7 cell, which may be mediated by the phosphorylation of ERK1/2.