CAJ | 학술논문

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。
목적：탐토거서세포이동억제인자（MIF）촉혈관평활기세포효원합성적가능신호전도도경。방법체외분별용MIF、혈관긴장소Ⅱ（AngⅡ）、MIF ＋PD 98059、AngⅡ＋PD 98059작용우대서주동맥혈관평활기세포，통과 Western-blotting 방법관찰평활기세포외조절단백격매（ERK）린산화수평。결과MIF、AngⅡ자격평활기세포，제시2조린산화 ERK 함량명현증가（P ＜0．05），AngⅡ조린산화 ERK 함량고우 MIF 조。가입 PD98059억제 ERK 신호통로후，2조린산화 ERK 함량명현강저（P＜0．05）。결론MIF、AngⅡ균가이격활 MAPK/ERK 도경，제시 MIF 대효원적합성적신호전도통로여 AngⅡ대효원적합성적신호전도통로가능시상동적。
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,AngⅡ +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 Ang II 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.