Activation of c-Jun N-terminal kinase by cadmium in mouse embryo neural cells in vitro

Environmental Toxicology and Pharmacology
Katharine M W Haberstroh, C M Kapron

Abstract

Members of the c-Jun NH(2)-terminal kinase (JNK) signalling pathway have been found to be stimulated by a variety of stresses, including heavy metals, hyperthermia, and UV-irradiation. In the present study, we examined whether exposure of micromass cultures of mouse embryonic midbrain cells to a known teratogen, cadmium, leads to the phosphorylation and activation of JNK. Midbrain cells exposed to 0.5, 1, 2, or 4μM cadmium chloride (CdCl(2)) showed a dose-dependent decline in cell numbers, cell viability and differentiation after 5 days. In cells exposed to 4μM CdCl(2) for up to 1h, the level of phosphorylated JNK increased by 15min and peaked at 30min exposure time, as determined by a phospho-specific anti-JNK antibody, while the total amount of JNK protein did not change. This phosphorylated JNK was active, as shown by a corresponding increase in the level of c-Jun phosphorylated on Ser63 in a kinase assay. These results demonstrate that CdCl(2) induces a rapid and transient activation of the JNK pathway in primary embryonic neuron cell cultures.

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Related Concepts

Cadmium
Cell Differentiation Process
Cell Survival
Malignant Hyperpyrexia due to Anesthesia
Midbrain Structure
Laboratory mice
Neurons
Phosphorylation
Signal Pathways
Cadmium chloride

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