巨噬细胞移动抑制因子对血管平滑肌细胞胶原代谢信号转导的影响  

Influence of macrophage migration inhibitory factor on signal transmit mechanism of collagen metabolism in vascular smooth muscle cell

作　　者：章玲[1] 李军[1] 麦爱欢[1] 梁新剑[1] 

机构地区：[1]广东省深圳市人民医院心内科,广东深圳518000

出　　处：《实用临床医药杂志》2014年第7期11-13,共3页Journal of Clinical Medicine in Practice

基　　金：广东省深圳市科技计划项目(200702002)

摘　　要：目的探讨巨噬细胞移动抑制因子(MIF)促血管平滑肌细胞胶原合成的可能信号转导途径。方法体外分别用MIF、血管紧张素Ⅱ(AngⅡ)、MIF+PD 98059、AngⅡ+PD 98059作用于大鼠主动脉血管平滑肌细胞,通过Western-blotting方法观察平滑肌细胞外调节蛋白激酶(ERK)磷酸化水平。结果 MIF、AngⅡ刺激平滑肌细胞,提示2组磷酸化ERK含量明显增加(P<0.05),AngⅡ组磷酸化ERK含量高于MIF组。加入PD98059抑制ERK信号通路后,2组磷酸化ERK含量明显降低(P<0.05)。结论 MIF、AngⅡ均可以激活MAPK/ERK途径,提示MIF对胶原的合成的信号转导通路与AngⅡ对胶原的合成的信号转导通路可能是相同的。Objective To explore the influence of macrophage migration inhibitory factor （MIF） on signal transmit route of collagen synthesis in vascular smooth muscle cell （SMC）. Methods The expression of signal transmit phosphorylated ERK of SMC in the rat aorta was measured by the western blotting procession after stimulation by MIF, Ang Ⅱ, MIF ＋ PD 98059, Ang Ⅱ ＋ PD 98059. Results The expression of phosphate ERK of the SMC raised significantly after MIF and Ang Ⅱ stim- ulation （P 〈 0.05）. The mount of phosphorylated ERK in the Ang II group was higher than that in the MIF group. After adding PD 98059, the phosphorylated ERK in both groups decreased significantly （P 〈 0.05）. Conclusion Both MIF and AngⅡ can activate MAPK/ERK route, and it might act in the same signal transmit route of collagen synthesis between MIF effect and Ang II effect.

关 键 词：巨噬细胞移动抑制因子 平滑肌细胞 胶原 信号转导通路 细胞外调节蛋白激酶 

分 类 号：R337.3[医药卫生—人体生理学]