近年来多发伤的发生率逐年提高,严重程度逐步加剧,伤情也日趋复杂。创伤后脓毒血症及多器官功能障碍综合征（multiple organ dysfunction syndrome,MODS）的发生率和死亡率也随之升高[1-2],我国每年因创伤致死的人数上升至人口死因的第...近年来多发伤的发生率逐年提高,严重程度逐步加剧,伤情也日趋复杂。创伤后脓毒血症及多器官功能障碍综合征（multiple organ dysfunction syndrome,MODS）的发生率和死亡率也随之升高[1-2],我国每年因创伤致死的人数上升至人口死因的第4-5位。内皮祖细胞（endothelial progenitor cell,EPC）是1997年由Asahara等[3]首先从外周血液单个核细胞中分离出的一种祖细胞群,具有增殖、迁徙和分化为成熟内皮细胞的能力。展开更多
Slit2/Robo1 is a conserved ligand-receptor system,which greatly affects the distribution,migration,axon guidance and branching of neuron cells.Slit2 and its transmembrane receptor Robo1 have different distribution pat...Slit2/Robo1 is a conserved ligand-receptor system,which greatly affects the distribution,migration,axon guidance and branching of neuron cells.Slit2 and its transmembrane receptor Robo1 have different distribution patterns in gliomas.The expression of Slit2 is at very low levels in pilocytic astrocytoma,fibrillary astrocytoma and glioblastoma,while Robo1 is highly expressed in different grades of gliomas at both mRNA and protein levels.Acquisition of insidious invasiveness by malignant glioma cells involves multiple genetic alterations in signaling pathways.Although the specific mechanisms of tumor-suppressive effect of Slit2/Robo1 have not been elucidated,it has been proved that Slit2/Robo1 signaling inhibits glioma cellmigration and invasion by inactivation of Cdc42-GTP.With the research development on the molecular mechanisms of Slit2/Robo1 signaling in glioma invasion and migration,Slit2/Robo1 signaling may become a potential target for glioma prevention and treatment.展开更多
文摘目的探讨Slit2/Robo4信号通路在神经元迁移中的活力与凋亡影响,为阐明脑缺血后神经血管新生的机制提供理论和实验依据。方法选择成年雄性远交群（SD）大鼠,建立缺血性脑卒中动物模型,采用Western blot方法测定梗死侧与非梗死侧Slit2和Robo4的表达。取原代培养10-14d的神经元种六孔板,分为加药组H2O2（100μmol/L）、对照组、H2O2（100μmol/L）＋Slit2（3μg/mL）组,行MTT方法检测细胞活力与双染流式细胞术检测细胞凋亡情况。结果 Western blot结果显示,梗死侧Slit2和Robo4表达均较非梗死侧明显升高,差异有统计学意义（P〈0.05）。100μmol/L H2O2处理原代培养神经元24h会导致Slit2和Robo4表达升高（P〈0.05）。MTT结果示,H2O2、H2O2＋Slit2组细胞活力都有明显下降,其中,H2O2＋Slit2组的细胞存活率明显高于单纯H2O2组（P〈0.05）。流式细胞学显示,H2O2＋Slit2组的细胞凋亡率明显低于H2O2组,差异有统计学意义（P〈0.05）。结论缺血性脑卒中有内源性Slit2/Robo4信号通路的激活,而外源性Slit2可以促进氧化应激时神经元的存活能力,抑制其凋亡作用,从而起到神经保护作用。
基金supported by the grants of National Natural Science Foundation of China(No.30700253,30800355)the Program for Changjiang Scholars and Innovative Research Team in University,Ministry of Education,China(No.IRT0734)
文摘Slit2/Robo1 is a conserved ligand-receptor system,which greatly affects the distribution,migration,axon guidance and branching of neuron cells.Slit2 and its transmembrane receptor Robo1 have different distribution patterns in gliomas.The expression of Slit2 is at very low levels in pilocytic astrocytoma,fibrillary astrocytoma and glioblastoma,while Robo1 is highly expressed in different grades of gliomas at both mRNA and protein levels.Acquisition of insidious invasiveness by malignant glioma cells involves multiple genetic alterations in signaling pathways.Although the specific mechanisms of tumor-suppressive effect of Slit2/Robo1 have not been elucidated,it has been proved that Slit2/Robo1 signaling inhibits glioma cellmigration and invasion by inactivation of Cdc42-GTP.With the research development on the molecular mechanisms of Slit2/Robo1 signaling in glioma invasion and migration,Slit2/Robo1 signaling may become a potential target for glioma prevention and treatment.
