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p38 and Extracellular Signal‐Regulated Kinases Activations have Opposite Effects on Primary‐Cultured Rat Cerebellar Granule Neurons Exposed to Sodium Arsenite
Author(s) -
Liu Xiaona,
Gao Yanhui,
Yao Hongju,
Zhou Lingwang,
Pei Junrui,
Sun Liyan,
Wang Jing,
Sun Dianjun
Publication year - 2014
Publication title -
journal of biochemical and molecular toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.526
H-Index - 58
eISSN - 1099-0461
pISSN - 1095-6670
DOI - 10.1002/jbt.21546
Subject(s) - sodium arsenite , p38 mitogen activated protein kinases , kinase , arsenite , extracellular , viability assay , microbiology and biotechnology , apoptosis , chemistry , phosphorylation , mapk/erk pathway , biology , biochemistry , arsenic , organic chemistry
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.