Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/17980
Title: p38 and ERK, but not JNK, are involved in copper-induced apoptosis in cultured cerebellar granule neurons
Authors: Chen, X
Lan, X
Mo, S
Qin, J
Li, W
Liu, P
Han, Y 
Pi, R
Keywords: Cerebellar granule neurons
Copper
Mitogen-activated protein kinases
Nimodipine
Reactive oxygen species
Issue Date: 2009
Publisher: Academic Press
Source: Biochemical and biophysical research communications, 2009, v. 379, no. 4, p. 944-948 How to cite?
Journal: Biochemical and biophysical research communications 
Abstract: Copper (Cu 2+) is an essential element for a variety of cellular functions; however, it is involved in neurotoxic events at excessive doses. Mechanisms of Cu 2+-induced neurotoxicity are not well understood. Here, we studied the toxic effects of Cu 2+ on cultured cerebellar granule neurons (cCGNs). Treatment of cCGNs with CuCl 2 (50 and 75 μM) caused a concentration- and time-dependent cell death with apoptotic characters, including chromatin condensation and DNA ladder. Cu 2+ potently induced reactive oxygen species (ROS), and quickly and slightly increased the intracellular concentration of calcium. Western blot assay showed that Cu 2+ increased phosphorylation of p38 mitogen-activated protein kinase (MAPK) and ERK1/2, but not that of JNK-1. Pharmacological inhibition of calcium influx, p38 MAPK and ERK1/2 attenuated the Cu 2+ toxicity in cCGNs. These findings demonstrate that p38 MAPK and ERK1/2, but not JNK, are involved in apoptosis of cCGNs induced by copper, and p38 and ERK may be the downstream effectors of ROS and calcium signaling.
URI: http://hdl.handle.net/10397/17980
ISSN: 0006-291X
EISSN: 1090-2104
DOI: 10.1016/j.bbrc.2008.12.177
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