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Induction of heat shock proteins (HSPs) by sodium arsenite in cultured astrocytes and reduction of hydrogen peroxide‐induced cell death
Author(s) -
Fauconneau Bernard,
Petegnief Valérie,
Sanfeliu Coral,
Piriou Alain,
Planas Anna M.
Publication year - 2002
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.2002.01230.x
Subject(s) - sodium arsenite , protein kinase b , programmed cell death , arsenite , apoptosis , oxidative stress , tunel assay , microbiology and biotechnology , heat shock protein , hsp27 , chemistry , protein kinase a , biology , kinase , biochemistry , hsp70 , arsenic , organic chemistry , gene
Induction of heat shock proteins (HSPs) protects cells from oxidative injury. Here Hsp72, Hsp27 and heme oxygenase‐1 (HO‐1) were induced in cultured rat astrocytes, and protection against oxidative stress was investigated. Astrocytes were treated with sodium arsenite (20–50 µ m ) for 1 h, which was non‐toxic to cells, 24 h later they were exposed to 400 µ m H 2 O 2 for 1 h, and cell death was evaluated at different time points. Arsenite triggered strong induction of HSPs, which was prevented by 1 µg/mL cycloheximide (CXH). H 2 O 2 caused cell loss and increased cell death with features of apoptosis, i.e. TdT‐mediated dUTP nick‐end labelling (TUNEL) reaction and caspase‐3 activation. These features were abrogated by pre‐treatment with arsenite, which prevented cell loss and significantly reduced the number of dead cells. The protective effect of arsenite was not detected in the presence of CHX. Pre‐treatment with arsenite increased protein kinase B (Akt) and extracellular signal regulated kinase 1/2 (ERK1/2) phosphorylation after H 2 O 2 . However, while Akt phosphorylation was prevented by CHX, Erk1/2 phosphorylation was further enhanced by CHX. The results show that transient arsenite pre‐treatment induces Hsp72, HO‐1 and, to a lesser extent, Hsp27; it reduces H 2 O 2 ‐induced astrocyte death; and it causes selective activation of Akt following H 2 O 2 . It is suggested that HSP expression at the time of H 2 O 2 exposure protects astrocytes from oxidative injury and apoptotic cell death by means of pro‐survival Akt.