The neuroprotective effect of heme oxygenase (HO) on oxidative stress in HO-1 siRNA-transfected HT22 cells

To investigate the role of heme oxygenase (HO) isozymes, we used siRNA technology to suppress HO-1 expression. HO-1 siRNA-transfected HT22 cells were vulnerable to hydrogen peroxide- and 4-hydroxynonenal-induced cytotoxicity. Biliverdin and bilirubin, degradative products of heme catalyzed by HO, pr...

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Bibliographic Details
Published in:Brain research 2006-09, Vol.1108 (1), p.39-44
Main Authors: Kaizaki, Asuka, Tanaka, Sachiko, Ishige, Kumiko, Numazawa, Satoshi, Yoshida, Takemi
Format: Article
Language:English
Subjects:
Aldehydes - toxicity
Animals
Bilirubin
Biological and medical sciences
Brain - enzymology
Brain - physiopathology
Cell Line, Transformed
Down-Regulation - genetics
Gene Silencing - physiology
Heme oxygenase
Heme Oxygenase-1 - genetics
HT22 cell
Hydrogen Peroxide - toxicity
Medical sciences
Mice
Neurodegenerative Diseases - enzymology
Neurodegenerative Diseases - genetics
Neurodegenerative Diseases - physiopathology
Neuronal cell death
Neuropharmacology
Neuroprotective agent
Neuroprotective Agents - metabolism
Oxidative stress
Oxidative Stress - drug effects
Oxidative Stress - genetics
Pharmacology. Drug treatments
RNA Interference
siRNA
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Summary:To investigate the role of heme oxygenase (HO) isozymes, we used siRNA technology to suppress HO-1 expression. HO-1 siRNA-transfected HT22 cells were vulnerable to hydrogen peroxide- and 4-hydroxynonenal-induced cytotoxicity. Biliverdin and bilirubin, degradative products of heme catalyzed by HO, protected HT22 cells from the insult of these oxidative stressors. These results suggest that inducible HO-1 plays a protective role against oxidative stress in HT22 cells.
ISSN:0006-8993
1872-6240
DOI:10.1016/j.brainres.2006.06.011