Differential regulation of map kinase isoforms by H2O2 in neuronal cells

Amandeep Gargi, Naresh Kumar, C. Dey
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Abstract

The mitogen-activated protein kinase (MAPK) family is involved in the regulation of cellular proliferation, differentiation and stress signals. In this study, we investigated the role of MAPK in response to H2O2, an oxidative stress, in neuronal cells. Activation of c-Jun-N-terminal kinase (JNK) was sustained, where as extracellular signal-regulated kinase (ERK) and p38 MAPK were transiently activated in response to H2O2 treatment. Inhibition of ERK and p38 resulted in higher activation of JNK in response to H2O2 treatment. The treatment with H2O2 led to apoptosis. The results implicate potential role of MAP kinases in neurodegenerative disorders mediated by oxidative stress.
H2O2对神经元细胞中map激酶同种异构体的差异调节
丝裂原活化蛋白激酶(MAPK)家族参与细胞增殖、分化和应激信号的调控。在这项研究中,我们研究了MAPK在神经元细胞中响应H2O2(一种氧化应激)的作用。c- jun - n末端激酶(JNK)被持续激活,其中细胞外信号调节激酶(ERK)和p38 MAPK在H2O2处理下被短暂激活。抑制ERK和p38导致JNK在H2O2处理下的高活化。H2O2处理导致细胞凋亡。结果提示MAP激酶在氧化应激介导的神经退行性疾病中的潜在作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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