M-CSF促进RAW 264.7细胞MMP-9的分泌及其可能机制  

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

作　　者：王春[1] 许灿新[1] 彭翠英[1] 秦旭平[1] 李凯[1] 廖端芳[1] 

机构地区：[1]南华大学药物药理研究所,南华大学护理学院湖南衡阳421001

出　　处：《中国药理学通报》2006年第8期947-951,共5页Chinese Pharmacological Bulletin

基　　金：国家自然科学基金资助课题(No30470719)

摘　　要：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。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 PI）98059 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.

关 键 词：巨噬细胞集落刺激因子 基质金属蛋白酶 细胞外信号调节激酶1/2 动脉粥样硬化 巨噬细胞 

分 类 号：R329.2[医药卫生—人体解剖和组织胚胎学] R329.24[医药卫生—基础医学]