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  • Title: p38 and ERK, but not JNK, are involved in copper-induced apoptosis in cultured cerebellar granule neurons.
    Author: Chen X, Lan X, Mo S, Qin J, Li W, Liu P, Han Y, Pi R.
    Journal: Biochem Biophys Res Commun; 2009 Feb 20; 379(4):944-8. PubMed ID: 19138669.
    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 75muM) 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.
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