Journal
JOURNAL OF TRACE ELEMENTS IN MEDICINE AND BIOLOGY
Volume 29, Issue -, Pages 275-283Publisher
ELSEVIER GMBH, URBAN & FISCHER VERLAG
DOI: 10.1016/j.jtemb.2014.06.006
Keywords
Cadmium; Apoptosis; Mitochondrial apoptotic pathway; Mitogen-activated protein kinase; Primary rat cerebral cortical neurons
Funding
- National Natural Science Foundation of China [31101866, 31172373, 31372495, 31302058]
- Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD)
- Graduate Innovation Project of Jiangsu Province [CXZZ13_0914]
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Cadmium (Cd) is an extremely toxic metal capable of severely damaging several organs, including the brain. Studies have shown that Cd induces neuronal apoptosis partially by activating the mitogen-activated protein kinase (MAPK) pathways. However, the underlying mechanism of MAPK involving the mitochondria] apoptotic pathway in neurons remains unclear. In this study, primary rat cerebral cohical neurons were exposed to Cd, which significantly decreased cell viability and the B-cell lymphoma 2/Bcl-2 associate X protein (Bcl-2/Bax) ratio and increased the percentage of apoptotic cells, release of cytochrome c, cleavages of caspase-3 and poly (ADP-ribose) polymerase (PARP), and nuclear translocation of apoptosis-inducing factor (AIF). In addition, Cd induced phosphorylation of extracellular signal-regulated kinase (ERIC), c-Jun N-terminal kinase (JNK) and p38 MAPK. Inhibition of ERIC and JNK, but not p38 MAPK, partially protected the cells from Cd-induced apoptosis. ERIC and JNK inhibition also blocked alteration of the Bcl-2/Bax ratio, release of cytochrome c, cleavages of caspase-3 and PARP, and nuclear translocation of AIF. Taken together, these data suggest that the ERK- and JNK-mediated mitochondrial apoptotic pathways play important roles in Cd-induced neuronal apoptosis. (C) 2014 Elsevier GmbH. All rights reserved.
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