期刊
TOXICOLOGY IN VITRO
卷 27, 期 1, 页码 492-498出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.tiv.2012.07.007
关键词
p38 MAP kinase; ERK; Nitric oxide; Mouse embryonic stem cells; Apoptosis
类别
资金
- National Research Foundation of Korea (NRF)
- Ministry of Education, Science and Technology [2009-0075373, 2010-0006901, 2011-0018393]
- Korea government (MEST) [2011-0030761]
- National Research Foundation of Korea [2011-0030121, 2009-0075373, 2011-0030761, 2010-0006901] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Previous study showed that nitric oxide (NO) induces apoptosis in mouse embryonic stem (mES) cells, but the precise mechanism governing NO-induced apoptosis in mES remains unclear. This study investigated the mechanism of NO-induced apoptosis of mES cells via MAP kinase signaling pathway. Sodium nitroprusside (SNP), a NO donor, induced apoptosis in mES cells with enhanced production of reactive oxygen species (ROS). In addition, treatment with SNP induced the activation of caspase-3, -8 and -9 as well as mitogen-activated protein (MAP) kinases (INK, p38 MAP kinase and ERK). However, pretreatment with the p38 MAP kinase inhibitor SB203580 and ERK inhibitor U0126 attenuated NO-induced cell toxicity, ROS production, and caspase-3 activation. Moreover, SB203580 inhibited the translocation of Bax from the cytosol to the mitochondria. Taken together, these results suggest that NO-induced apoptosis in mES cells was mediated through p38 MAP kinase/ERK signaling pathway by triggering caspases activation and Bax translocation from the cytosol to the mitochondria. (C) 2012 Elsevier Ltd. All rights reserved.
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