辐射诱导IEC-6细胞MAPK信号转导途径的激活(英文)  

RADIATION-INDUCED ACTIVATION OF THE MITOGEN-ACTIVATED PROTEIN KINASE SIGNAL TRANSDUCTION PATHWAY IN IEC-6 CELLS

作　　者：周舟[1] 王小华[1] Igisu Hideki 林远[1] 楼淑芬[1] Matsuoka Masato 程天民[1] 余争平[1] 

机构地区：[1]第三军医大学复合伤研究所,重庆400038 [2]日本产业医科大学环境毒理研究室,日本北九州市80785555

出　　处：《辐射研究与辐射工艺学报》2002年第2期137-145,共9页Journal of Radiation Research and Radiation Processing

基　　金：~~

摘　　要：研究检测了γ辐射对IEC 6肠上皮细胞丝裂原激活的蛋白激酶 (MAPKS)的激活效应。 6Gyγ辐射未引起ERK蛋白磷酸化的显著改变 ,而辐照射后 30minJNK与 p38MAPK蛋白磷酸化显著增强 ,ERK、JNK和p38MAPK的总蛋白表达水平未见明显的变化。受照后 12h细胞存活率显著降低。螯合细胞内Ca2 +可几乎完全抑制γ辐照引起的JNK与 p38MAPK的蛋白磷酸化 ,而清除细胞外Ca2 +却无此作用。p38MAPK的激活与γ辐射诱导的细胞凋亡显著相关 ,而ERK则无明显的关联。实验结果表明 ,γ辐射是一种强的JNK与 p38MAPK激活因素 ,并且细胞内储存Ca2 +的释放在γ辐射诱导的IECEffects of γ irradiation on mitogen activated protein kinases (MAPKs) were examined in IEC 6 cells.In response to γ irradiation,Phosphorylation of intracellular signal regulated protein kinase (ERK) was not significantly altered.The levels of phosphorylated forms of c Jun NH 2 terminal kinase (JNK) and p38 MAPK increased at 30 min following exposure to 6Gy γ irradiation,while the cell viability was lowered significantly at 12h.On the other hand,no clear changes were found in the total protein levels of ERK,JNK and p38 MAPK.Chelation of intracellular Ca 2+ suppressed γ irradiation induced JNK and p38 MAPK phosphorylation almost completely,but removal of external Ca 2+ did not.Activation of p38MAPK, but not ERK,was correlated with γ irradiation induced apoptosis.The present results showed that γ irradiation is a potent activator of JNK and p38 MAPK,and Ca 2+ mobilized from intracellular stores plays an important role for the activation of MAPKs and the induction of apoptosis in IEC 6 cells.

关 键 词：Γ辐射 ERK JNK P38MAPK IEC-6细胞 蛋白激酶 蛋白磷酸化 激活效应 辐射诱导 信号转导途径 

分 类 号：Q274[生物学—细胞生物学] R811[医药卫生—放射医学]