p38 and ERK, but not JNK, are involved in copper-induced apoptosis in cultured cerebellar granule neurons

Xiaohong Chen, Xiujian Lan, Suilin Mo, Jian Qin, Wenming Li, Peiqing Liu, Yifan Han, Rongbiao Pi

Research output: Journal article publicationJournal articleAcademic researchpeer-review

35 Citations (Scopus)


Copper (Cu2+) is an essential element for a variety of cellular functions; however, it is involved in neurotoxic events at excessive doses. Mechanisms of Cu2+-induced neurotoxicity are not well understood. Here, we studied the toxic effects of Cu2+on cultured cerebellar granule neurons (cCGNs). Treatment of cCGNs with CuCl2(50 and 75 μM) caused a concentration- and time-dependent cell death with apoptotic characters, including chromatin condensation and DNA ladder. Cu2+potently induced reactive oxygen species (ROS), and quickly and slightly increased the intracellular concentration of calcium. Western blot assay showed that Cu2+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 Cu2+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.
Original languageEnglish
Pages (from-to)944-948
Number of pages5
JournalBiochemical and Biophysical Research Communications
Issue number4
Publication statusPublished - 20 Feb 2009


  • Cerebellar granule neurons
  • Copper
  • Mitogen-activated protein kinases
  • Nimodipine
  • Reactive oxygen species

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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