Protective role of heme oxygenase-1 in oxidative stress-induced neuronal injury

Weidong Le; Wen Jie Xie; Stanley H. Appel

doi:10.1002/(SICI)1097-4547(19990615)56:6<652::AID-JNR11>3.0.CO;2-5

Protective role of heme oxygenase-1 in oxidative stress-induced neuronal injury

Weidong Le, Wen Jie Xie, Stanley H. Appel

Research output: Contribution to journal › Article › peer-review

147 Scopus citations

Abstract

Heme oxygenase-1 (HO-1) is a stress protein induced in response to a variety of oxidative challenges. After treatment of the hybrid septal cells SN 56 with β-amyloid peptide (β-AP_1-40) or hydrogen peroxide (H₂O₂), we detected high levels of reactive oxygen species, accompanied by a significant elevation in HO-1 expression. Levels of HO-1 increased and then decreased following cell loss. Pretreatment of SN 56 cells with HO-1 antisense oligonucleotides dramatically decreased the immunoreactivity of HO- 1 and significantly enhanced the cytotoxicity of β-AP_1-40 and H₂O₂. In contrast, pretreatment with hemin, an HO-1 inducer, increased the expression of HO-1 and decreased the β-AP_1-40- and H₂O₂-induced cytotoxicity. These findings support the importance of HO-1 in protecting neurons against oxidative stress-induced injury.

Original language	English (US)
Pages (from-to)	652-658
Number of pages	7
Journal	Journal of Neuroscience Research
Volume	56
Issue number	6
DOIs	https://doi.org/10.1002/(SICI)1097-4547(19990615)56:6<652::AID-JNR11>3.0.CO;2-5
State	Published - Jun 15 1999

Keywords

β-Amyloid
Alzheimer's disease
Antioxidant
Hydrogen peroxide

ASJC Scopus subject areas

Neuroscience(all)

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10.1002/(SICI)1097-4547(19990615)56:6<652::AID-JNR11>3.0.CO;2-5

Cite this

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title = "Protective role of heme oxygenase-1 in oxidative stress-induced neuronal injury",

abstract = "Heme oxygenase-1 (HO-1) is a stress protein induced in response to a variety of oxidative challenges. After treatment of the hybrid septal cells SN 56 with β-amyloid peptide (β-AP1-40) or hydrogen peroxide (H2O2), we detected high levels of reactive oxygen species, accompanied by a significant elevation in HO-1 expression. Levels of HO-1 increased and then decreased following cell loss. Pretreatment of SN 56 cells with HO-1 antisense oligonucleotides dramatically decreased the immunoreactivity of HO- 1 and significantly enhanced the cytotoxicity of β-AP1-40 and H2O2. In contrast, pretreatment with hemin, an HO-1 inducer, increased the expression of HO-1 and decreased the β-AP1-40- and H2O2-induced cytotoxicity. These findings support the importance of HO-1 in protecting neurons against oxidative stress-induced injury.",

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author = "Weidong Le and Xie, {Wen Jie} and Appel, {Stanley H.}",

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AU - Le, Weidong

AU - Xie, Wen Jie

AU - Appel, Stanley H.

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N2 - Heme oxygenase-1 (HO-1) is a stress protein induced in response to a variety of oxidative challenges. After treatment of the hybrid septal cells SN 56 with β-amyloid peptide (β-AP1-40) or hydrogen peroxide (H2O2), we detected high levels of reactive oxygen species, accompanied by a significant elevation in HO-1 expression. Levels of HO-1 increased and then decreased following cell loss. Pretreatment of SN 56 cells with HO-1 antisense oligonucleotides dramatically decreased the immunoreactivity of HO- 1 and significantly enhanced the cytotoxicity of β-AP1-40 and H2O2. In contrast, pretreatment with hemin, an HO-1 inducer, increased the expression of HO-1 and decreased the β-AP1-40- and H2O2-induced cytotoxicity. These findings support the importance of HO-1 in protecting neurons against oxidative stress-induced injury.

AB - Heme oxygenase-1 (HO-1) is a stress protein induced in response to a variety of oxidative challenges. After treatment of the hybrid septal cells SN 56 with β-amyloid peptide (β-AP1-40) or hydrogen peroxide (H2O2), we detected high levels of reactive oxygen species, accompanied by a significant elevation in HO-1 expression. Levels of HO-1 increased and then decreased following cell loss. Pretreatment of SN 56 cells with HO-1 antisense oligonucleotides dramatically decreased the immunoreactivity of HO- 1 and significantly enhanced the cytotoxicity of β-AP1-40 and H2O2. In contrast, pretreatment with hemin, an HO-1 inducer, increased the expression of HO-1 and decreased the β-AP1-40- and H2O2-induced cytotoxicity. These findings support the importance of HO-1 in protecting neurons against oxidative stress-induced injury.

KW - β-Amyloid

KW - Alzheimer's disease

KW - Antioxidant

KW - Hydrogen peroxide

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Protective role of heme oxygenase-1 in oxidative stress-induced neuronal injury

Abstract

Keywords

ASJC Scopus subject areas

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