Role of heme oxygenase‐1 in the regulation of manganese superoxide dismutase gene expression in oxidatively‐challenged astroglia
Identifieur interne : 002958 ( Main/Corpus ); précédent : 002957; suivant : 002959Role of heme oxygenase‐1 in the regulation of manganese superoxide dismutase gene expression in oxidatively‐challenged astroglia
Auteurs : Dov Frankel ; Khalil Mehindate ; Hyman M. SchipperSource :
- Journal of Cellular Physiology [ 0021-9541 ] ; 2000-10.
Abstract
Manganese superoxide dismutase (MnSOD) is an antioxidant enzyme that reduces superoxide anion to hydrogen peroxide in cell mitochondria. MnSOD is overexpressed in normal aging brain and in various central nervous system disorders; however, the mechanisms mediating the upregulation of MnSOD under these conditions remain poorly understood. We previously reported that cysteamine (CSH) and other pro‐oxidants rapidly induce the heme oxygenase‐1 (HO‐1) gene in cultured rat astroglia followed by late upregulation of MnSOD in these cells. In the present study, we demonstrate that antecedent upregulation of HO‐1 is necessary and sufficient for subsequent induction of the MnSOD gene in neonatal rat astroglia challenged with CSH or dopamine, and in astroglial cultures transiently transfected with full‐length human HO‐1 cDNA. Treatment with potent antioxidants attenuates MnSOD expression in HO‐1–transfected astroglia, strongly suggesting that intracellular oxidative stress signals MnSOD gene induction in these cells. Activation of this HO‐1‐MnSOD axis may play an important role in the pathogenesis of Alzheimer disease, Parkinson disease and other free radical‐related neurodegenerative disorders. In these conditions, compensatory upregulation of MnSOD may protect mitochondria from oxidative damage accruing from heme‐derived free iron and carbon monoxide liberated by the activity of HO‐1. J. Cell. Physiol. 185:80–86, 2000. © 2000 Wiley‐Liss, Inc.
Url:
DOI: 10.1002/1097-4652(200010)185:1<80::AID-JCP7>3.0.CO;2-W
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MnSOD is overexpressed in normal aging brain and in various central nervous system disorders; however, the mechanisms mediating the upregulation of MnSOD under these conditions remain poorly understood. We previously reported that cysteamine (CSH) and other pro‐oxidants rapidly induce the heme oxygenase‐1 (HO‐1) gene in cultured rat astroglia followed by late upregulation of MnSOD in these cells. In the present study, we demonstrate that antecedent upregulation of HO‐1 is necessary and sufficient for subsequent induction of the MnSOD gene in neonatal rat astroglia challenged with CSH or dopamine, and in astroglial cultures transiently transfected with full‐length human HO‐1 cDNA. Treatment with potent antioxidants attenuates MnSOD expression in HO‐1–transfected astroglia, strongly suggesting that intracellular oxidative stress signals MnSOD gene induction in these cells. Activation of this HO‐1‐MnSOD axis may play an important role in the pathogenesis of Alzheimer disease, Parkinson disease and other free radical‐related neurodegenerative disorders. In these conditions, compensatory upregulation of MnSOD may protect mitochondria from oxidative damage accruing from heme‐derived free iron and carbon monoxide liberated by the activity of HO‐1. J. Cell. Physiol. 185:80–86, 2000. © 2000 Wiley‐Liss, Inc.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Dov Frankel</name><affiliations><json:string>Bloomfield Centre for Research in Aging, Lady Davis Institute for Medical Research, Sir Mortimer B. 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In the present study, we demonstrate that antecedent upregulation of HO‐1 is necessary and sufficient for subsequent induction of the MnSOD gene in neonatal rat astroglia challenged with CSH or dopamine, and in astroglial cultures transiently transfected with full‐length human HO‐1 cDNA. Treatment with potent antioxidants attenuates MnSOD expression in HO‐1–transfected astroglia, strongly suggesting that intracellular oxidative stress signals MnSOD gene induction in these cells. Activation of this HO‐1‐MnSOD axis may play an important role in the pathogenesis of Alzheimer disease, Parkinson disease and other free radical‐related neurodegenerative disorders. In these conditions, compensatory upregulation of MnSOD may protect mitochondria from oxidative damage accruing from heme‐derived free iron and carbon monoxide liberated by the activity of HO‐1. J. Cell. 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Activation of this HO‐1‐MnSOD axis may play an important role in the pathogenesis of Alzheimer disease, Parkinson disease and other free radical‐related neurodegenerative disorders. In these conditions, compensatory upregulation of MnSOD may protect mitochondria from oxidative damage accruing from heme‐derived free iron and carbon monoxide liberated by the activity of HO‐1. J. Cell. 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Davis‐Jewish General Hospital, Montreal, Canada</affiliation><affiliation>Departments of Neurology and Neurosurgery, and Medicine (Geriatrics), McGill University, Montreal, Canada</affiliation><description>Correspondence: Lady Davis Institute for Medical Research, 3755 Cote Ste. 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MnSOD is overexpressed in normal aging brain and in various central nervous system disorders; however, the mechanisms mediating the upregulation of MnSOD under these conditions remain poorly understood. We previously reported that cysteamine (CSH) and other pro‐oxidants rapidly induce the heme oxygenase‐1 (HO‐1) gene in cultured rat astroglia followed by late upregulation of MnSOD in these cells. In the present study, we demonstrate that antecedent upregulation of HO‐1 is necessary and sufficient for subsequent induction of the MnSOD gene in neonatal rat astroglia challenged with CSH or dopamine, and in astroglial cultures transiently transfected with full‐length human HO‐1 cDNA. Treatment with potent antioxidants attenuates MnSOD expression in HO‐1–transfected astroglia, strongly suggesting that intracellular oxidative stress signals MnSOD gene induction in these cells. Activation of this HO‐1‐MnSOD axis may play an important role in the pathogenesis of Alzheimer disease, Parkinson disease and other free radical‐related neurodegenerative disorders. In these conditions, compensatory upregulation of MnSOD may protect mitochondria from oxidative damage accruing from heme‐derived free iron and carbon monoxide liberated by the activity of HO‐1. J. Cell. Physiol. 185:80–86, 2000. © 2000 Wiley‐Liss, Inc.</abstract><note type="funding">Medical Research Council of Canada</note><note type="funding">Fonds de la recherche en santé du Québec</note><note type="funding">Alzheimer's Association (U.S.)</note><relatedItem type="host"><titleInfo><title>Journal of Cellular Physiology</title></titleInfo><titleInfo type="abbreviated"><title>J. Cell. 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