机械牵张力诱导成骨细胞骨保护素及其配体表达的信号转导途径初探  

Preliminary investigation of signal transduction pathway on expression levels of OPG/RANKL that mediated cellular responses to mechanical strain in MC3T3-E1 cells

作　　者：唐林[1] 赵红艳[1] 邵玶[1] 李永明[2] 林珠[2] 

机构地区：[1]哈尔滨医科大学口腔医学院正畸科,黑龙江哈尔滨150001 [2]第四军医大学口腔医学院正畸科,陕西西安710032

出　　处：《临床口腔医学杂志》2010年第4期202-204,共3页Journal of Clinical Stomatology

基　　金：龙江省教育厅科学技术研究项目(11521117);黑龙江省政府博士后基金资助(LRB08-545);哈尔滨医科大学附属第一医院科研基金(2007069)

摘　　要：目的:研究机械牵张力诱导成骨细胞OPG/RANKL表达变化的信号转导途径。方法:在MC3T3-E1细胞加力前半小时加入放线菌酮、吲哚美辛、染料木黄酮、PD098059等抑制剂,通过自制的多通道细胞牵张应力加载系统对细胞施加18%的机械牵张力,细胞的加载作用时间为24h。用RT-PCR方法检测细胞受力前后OPG/RANKL mRNA表达的变化,并进行统计分析。结果:吲哚美辛及染料木黄酮可抑制机械牵张力诱导的MC3T3-E1细胞OPG mRNA表达增加;PD098059可抑制机械牵张力诱导的MC3T3-E1细胞RANKL mRNA表达减少。结论:机械牵张力诱导的OPG表达增加可能是通过环氧合酶或者前列腺素合成途径,也可能是通过酪氨酸磷酸化途径,机械牵张力诱导RANKL表达的减少可能是通过ERK-MAPK途径。Objective：To investigate signal transduction pathway that mediated cellular responses to mechanical strain in MC3T3-E1 cells.Method：Inhibitors including cycloheximide,indomethacin,genistein,and PD 098059 were used.After the MC3T3-E1 cells had been pre-incubated in the presence of each inhibitor for 30 min to permit these compounds to penetrate the cells and block their respective pathways,cyclic tensile strain at 18 % elongation,6 cycles/min was applied in culture for 24 h,and the expression levels of OPG/RANKL mRNA were determined by RT-PCR.Result：The induction of OPG mRNA expression by stretching was inhibited by indomethacin or genistein,and the stretch-induced reduction of RANKL mRNA was inhibited by PD 098059.Conclusion：The signal transduction pathway that mediated cellular responses to mechanical strain in MC3T3-E1 cells are quite complex.This experiment indicates that the ERK-MAPK pathway is involved in RANKL expression.Moreover the induction of OPG mRNA by stretching in MC3T3-E1 cells is mediated by cyclooxygenase or prostaglandin synthesis,and the effect could in part involve an intracellular tyrosine kinase cascade.

关 键 词：机械牵张力 成骨细胞 骨保护素 骨保护素配体 

分 类 号：R782.2[医药卫生—口腔医学] Q813.1[医药卫生—临床医学]