Narang Himanshi, Bhat Nagesh, Gupta S K, Santra S, Choudhary R K, Kailash S, Krishna Malini
Radiation Biology and Health Sciences Division, Bhabha Atomic Research Centre, Trombay, Mumbai, 400085, India.
Mol Cell Biochem. 2009 Apr;324(1-2):85-91. doi: 10.1007/s11010-008-9987-y. Epub 2008 Dec 27.
Mitogen-activated protein kinases have been shown to respond to various stimuli including cytokines, mitogens and gamma irradiation, leading to cell proliferation, differentiation, or death. The duration of their activation determines the specificity of response to each stimulus in various cells. In this study, the crucial intracellular kinases, ERK, JNK, and p38 kinase involved in cell survival, death, or damage and repair were examined for their activity in RAW 264.7 cells at various time points after irradiation with 2 Gy doses of proton ions or X-rays. This is the first report that shows that the MAPK signaling induced after heavy ion or X-ray exposure is not the same. Unlike gamma irradiation, there was prolonged but marginal activation of prosurvival ERK pathway and significant activation of proapoptotic p38 pathway in response to high LET radiation.
丝裂原活化蛋白激酶已被证明可对包括细胞因子、丝裂原和γ射线照射在内的各种刺激作出反应,从而导致细胞增殖、分化或死亡。它们的激活持续时间决定了各种细胞对每种刺激反应的特异性。在本研究中,检测了参与细胞存活、死亡或损伤及修复的关键细胞内激酶ERK、JNK和p38激酶在2 Gy剂量的质子离子或X射线照射后不同时间点在RAW 264.7细胞中的活性。这是第一份表明重离子或X射线照射后诱导的MAPK信号传导不同的报告。与γ射线照射不同,高传能线密度辐射会导致促生存ERK途径的激活延长但程度轻微,同时促凋亡p38途径会显著激活。