降钙素基因相关肽／细胞外调节激酶信号通路对人MG-63细胞增殖的实验研究  

Calcitonin gene-related peptide promotes proliferation and differentiation of MG-63 cells via extracellular signal-regulated kinase pathway in vitro

作　　者：李岗[1] 王钢[1] 贾谊[1] 刘善宇[1] 

机构地区：[1]南方医科大学南方医院创伤骨科,广州510515

出　　处：《中华创伤骨科杂志》2011年第6期556-559,共4页Chinese Journal of Orthopaedic Trauma

摘　　要：目的研究外源性降钙素基因相关肽（CGRP）对人MG-63细胞增殖的影响及其可能涉及的信号通路。方法采用甲基噻唑基四唑（MTr）法和细胞计数法观察对比不同浓度外源性CGRP及其受体拮抗剂CGRP8．37与细胞外调解激酶（ERK）抑制剂PD98059对体外培养的人MG-63细胞增殖的影响。根据不同分组将体外培养的人MG-63细胞用CGRP、CGRP8-37及PD98059作用24h后，通过免疫细胞化学方法观察细胞骨保护蛋白（OPG）、护骨素配体（RANKL）、ERK表达强度的变化。结果不同浓度CGRP均可促进MG-63细胞的增殖，促进作用随浓度增高而增强，CGRP8-37、PD98059可减弱此作用，与对照组比较差异有统计学意义（P〈0．05）。CGRP呈剂量依赖性的上调成骨细胞OPG和ERK的表达，同时下调RANKL的表达，CGRP-37和PD98059可减弱此作用，与对照组比较差异有统计学意义（P〈0．05）。结论CGRP可通过ERK信号通路改变OPG／RANKL的比值来调控成骨细胞增殖。Objective To explore the effect of calcitonin gene-related peptide （CGRP） on proliferation and differentiation of MG-63 cells through extracellular signal-regulated kinase （ERK） pathway in vitro. Methods To study the effects of ERK inhibitor PD98059 and CGRP inhibitor CGRP8-37, 2 groups of MG-63 cells were treated with PD98059 and CGRP8-37 for one hour prior to serum treatment. The other 4 groups were cultured with serum of different doses （high, middle, low and blank）. Proliferation and apoptosis of MG-63 cells were observed by methyl thiazolyl tetrazolium （MTT） method and cell-counting. Expressions of osteoprotegerin （OPG）, receptor activator of nuclear factor kappaβ ligand （RANKL） and ERK were observed through immunocytoehemieal and image analysis. Results MTT showed that CGRP promoted proliferation of MG-63 cells and expressions of OPG and ERK but not expression of RANKL. The effect was dose-dependent, and significantly inhibited by either CGRP 8-37 or PD98059 （ P 〈 0.05） . Conclusion CGRP can stimulate proliferation of MG-63 cells via CGRP receptor and ERK pathway to regulate the ratio of OPG/RANKL.

关 键 词：降钙素基因相关肽 MG-63细胞 细胞增殖 

分 类 号：R285.5[医药卫生—中药学]