Jing Wang and Dianjun Sun contributed equally to the work.
p38 and Extracellular Signal-Regulated Kinases Activations have Opposite Effects on Primary-Cultured Rat Cerebellar Granule Neurons Exposed to Sodium Arsenite
Article first published online: 19 DEC 2013
© 2013 Wiley Periodicals, Inc.
Journal of Biochemical and Molecular Toxicology
Volume 28, Issue 4, pages 143–148, April 2014
How to Cite
Liu, X., Gao, Y., Yao, H., Zhou, L., Pei, J., Sun, L., Wang, J. and Sun, D. (2014), p38 and Extracellular Signal-Regulated Kinases Activations have Opposite Effects on Primary-Cultured Rat Cerebellar Granule Neurons Exposed to Sodium Arsenite. J. Biochem. Mol. Toxicol., 28: 143–148. doi: 10.1002/jbt.21546
Contract Grant Sponsor: National Natural Science Foundation of China.
Contract Grant Number: 81102082.
Contract Grant Sponsor: Natural Science Foundation of Heilongjiang Province of China
Contract Grant Number: D201053.
- Issue published online: 7 APR 2014
- Article first published online: 19 DEC 2013
- Manuscript Accepted: 24 NOV 2013
- Manuscript Revised: 6 NOV 2013
- Manuscript Received: 5 OCT 2013
- National Natural Science Foundation of China. Grant Number: 81102082
- Natural Science Foundation of Heilongjiang Province of China. Grant Number: D201053
- Sodium Arsenite;
- Rat Cerebellar Granule Neurons;
- Mitogen-Activated Protein Kinases
Arsenic is a widespread environmental toxicant in the world and regarded as both a carcinogen and an anticarcinogen. The present study was designed to evaluate roles of mitogen-activated protein kinases in sodium arsenite-induced effects on primary-cultured rat cerebellar granule neurons (CGNs). Results revealed a decreased viability of the cells exposed to sodium arsenite (from 0 to 50 μM) in a dose-dependent manner. Annexin V-fluorescein isothiocyanate assay showed that apoptosis was obviously induced by arsenite treatment. High phosphorylation expressions of p38 and extracellular signal-regulated kinases (ERK1/2), but not of c-Jun N-terminal kinases were observed due to arsenite treatment by western blotting analysis. Furthermore, SB203580 (an inhibitor of p38) decreased the percentage of apoptotic cells whereas arsenite-stimulated toxicity was enhanced by U0126 (an inhibitor of ERK1/2). Taken together, these data suggest that p38 contributes to arsenite-induced apoptosis of rat CGNs, but ERK1/2 may involve in cell growth and survival.