辐射诱导IEC-6细胞MAPK信号转导途径的激活

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与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。整． 螯合细胞内Ca^2 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Ca^2 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Ca^2 的释放在γ辐射诱导的IEC－6细胞MAPKs激活与细胞凋亡过程中起重要作用。

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

Effects of γ irradiation on mitogen-activated protein kinases(MAPKs) were examined in IEC-6 cells. In response to γ irradiation, Phosphoryla-tion of intracellular signal-regulated protein kinase (ERK) was not significantly al-tered. The levels of phosphorylated forms of c-Jun NH2-terminal kinase (JNK) andp38 MAPK increased at 30 min following exposure to 6Gy γ irradiation, while the cellviability was lowered significantly at 12h. On the other hand, no clear changes werefound in the total protein levels of ERK, JNK and p38 MAPK. Chelation of intra-cellular Ca2+ suppressed γ irradiation induced JNK and p38 MAPK phosphorylationalmost completely, but removal of external Ca2+ did not. Activation of p38MAPK.but not ERK, was correlated with γ irradiation induced apoptosis. The present resultsshowed that γ irradiation is a potent activator of JNK and p38 MAPK, and Ca2+ mo-bilized from intracellular stores plays an important role for the activation of MAPKsand the induction of apoptosis in IEC-6 cells.