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Stimulation of natriuretic peptide receptor C attenuates accumulation of reactive oxygen species and nitric oxide synthesis in ammonia‐treated astrocytes
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Zeitschriftentitel: | Journal of Neurochemistry |
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Personen und Körperschaften: | , , |
In: | Journal of Neurochemistry, 115, 2010, 4, S. 1068-1076 |
Format: | E-Article |
Sprache: | Englisch |
veröffentlicht: |
Wiley
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author_facet |
Skowrońska, Marta Zielińska, Magdalena Albrecht, Jan Skowrońska, Marta Zielińska, Magdalena Albrecht, Jan |
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author |
Skowrońska, Marta Zielińska, Magdalena Albrecht, Jan |
spellingShingle |
Skowrońska, Marta Zielińska, Magdalena Albrecht, Jan Journal of Neurochemistry Stimulation of natriuretic peptide receptor C attenuates accumulation of reactive oxygen species and nitric oxide synthesis in ammonia‐treated astrocytes Cellular and Molecular Neuroscience Biochemistry |
author_sort |
skowrońska, marta |
spelling |
Skowrońska, Marta Zielińska, Magdalena Albrecht, Jan 0022-3042 1471-4159 Wiley Cellular and Molecular Neuroscience Biochemistry http://dx.doi.org/10.1111/j.1471-4159.2010.07008.x <jats:sec><jats:label /><jats:p> <jats:italic>J. Neurochem.</jats:italic> (2010) <jats:bold>115</jats:bold>, 1068–1076.</jats:p></jats:sec><jats:sec><jats:title>Abstract</jats:title><jats:p>Oxidative and nitrosative stress contribute to ammonia‐induced astrocytic dysfunction in hepatic encephalopathy. Treatment of cultured astrocytes with 5 mmol/L ammonium chloride (‘ammonia’) increased the production of reactive oxygen species (ROS), including the toxic NADPH oxidase reaction product, •O<jats:sub>2</jats:sub><jats:sup>−</jats:sup>. Atrial natriuretic peptide (ANP), natriuretic peptide C and a selective natriuretic peptide receptor (NPR)‐C ligand, cANP<jats:sub>(4–23),</jats:sub> each decreased the total ROS content both in control cells and cells treated with ammonia. However, attenuation of •O<jats:sub>2</jats:sub><jats:sup>−</jats:sup> accumulation by ANP and cANP<jats:sub>(4–23),</jats:sub> was observed in ammonia‐treated cells only and the effect of cANP<jats:sub>(4–23)</jats:sub> was decreased when the NADPH oxidase‐regulatory protein G<jats:sub>iα‐2</jats:sub> was blocked with a specific anti‐G<jats:sub>iα‐2</jats:sub> antibody. Although in contrast to ANP, cANP<jats:sub>(4–23)</jats:sub> did not elevate the cGMP content in control astrocytes, it decreased cAMP content and reduced the expression of G<jats:sub>iα‐2</jats:sub>, the NADPH oxidase‐regulatory protein. The results show the presence of functional NPR‐C in astrocytes, activation of which (i) attenuates basal ROS production, and (ii) prevents excessive accumulation of the toxic ROS species, •O<jats:sub>2</jats:sub><jats:sup>−</jats:sup> by ammonia. Ammonia, ANP and cANP<jats:sub>(4–23)</jats:sub> added separately, each stimulated formation of NO<jats:sub>x</jats:sub> (nitrates + nitrites) which was associated with up‐regulation of the activity [cANP<jats:sub>(4–23)</jats:sub>] or/and expression (ammonia) of the endothelial isoform of nitric oxide synthase. However, the ammonia‐induced increase of NO<jats:sub>x</jats:sub> was not augmented by co‐addition of ANP, and was reduced to the control level by co‐addition of cANP<jats:sub>(4–23)</jats:sub>, indicating that activation of NPR‐C may also reduce nitrosative stress. Future hepatic encephalopathy therapy might include the use of cANP<jats:sub>(4–23)</jats:sub> or other NPR‐C agonists to control oxidative/nitrosative stress induced by ammonia.</jats:p></jats:sec> Stimulation of natriuretic peptide receptor C attenuates accumulation of reactive oxygen species and nitric oxide synthesis in ammonia‐treated astrocytes Journal of Neurochemistry |
doi_str_mv |
10.1111/j.1471-4159.2010.07008.x |
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Biologie Psychologie Chemie und Pharmazie |
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imprint |
Wiley, 2010 |
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Wiley, 2010 |
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skowronska2010stimulationofnatriureticpeptidereceptorcattenuatesaccumulationofreactiveoxygenspeciesandnitricoxidesynthesisinammoniatreatedastrocytes |
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2010 |
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Wiley |
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Journal of Neurochemistry |
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49 |
title |
Stimulation of natriuretic peptide receptor C attenuates accumulation of reactive oxygen species and nitric oxide synthesis in ammonia‐treated astrocytes |
title_unstemmed |
Stimulation of natriuretic peptide receptor C attenuates accumulation of reactive oxygen species and nitric oxide synthesis in ammonia‐treated astrocytes |
title_full |
Stimulation of natriuretic peptide receptor C attenuates accumulation of reactive oxygen species and nitric oxide synthesis in ammonia‐treated astrocytes |
title_fullStr |
Stimulation of natriuretic peptide receptor C attenuates accumulation of reactive oxygen species and nitric oxide synthesis in ammonia‐treated astrocytes |
title_full_unstemmed |
Stimulation of natriuretic peptide receptor C attenuates accumulation of reactive oxygen species and nitric oxide synthesis in ammonia‐treated astrocytes |
title_short |
Stimulation of natriuretic peptide receptor C attenuates accumulation of reactive oxygen species and nitric oxide synthesis in ammonia‐treated astrocytes |
title_sort |
stimulation of natriuretic peptide receptor c attenuates accumulation of reactive oxygen species and nitric oxide synthesis in ammonia‐treated astrocytes |
topic |
Cellular and Molecular Neuroscience Biochemistry |
url |
http://dx.doi.org/10.1111/j.1471-4159.2010.07008.x |
publishDate |
2010 |
physical |
1068-1076 |
description |
<jats:sec><jats:label /><jats:p> <jats:italic>J. Neurochem.</jats:italic> (2010) <jats:bold>115</jats:bold>, 1068–1076.</jats:p></jats:sec><jats:sec><jats:title>Abstract</jats:title><jats:p>Oxidative and nitrosative stress contribute to ammonia‐induced astrocytic dysfunction in hepatic encephalopathy. Treatment of cultured astrocytes with 5 mmol/L ammonium chloride (‘ammonia’) increased the production of reactive oxygen species (ROS), including the toxic NADPH oxidase reaction product, •O<jats:sub>2</jats:sub><jats:sup>−</jats:sup>. Atrial natriuretic peptide (ANP), natriuretic peptide C and a selective natriuretic peptide receptor (NPR)‐C ligand, cANP<jats:sub>(4–23),</jats:sub> each decreased the total ROS content both in control cells and cells treated with ammonia. However, attenuation of •O<jats:sub>2</jats:sub><jats:sup>−</jats:sup> accumulation by ANP and cANP<jats:sub>(4–23),</jats:sub> was observed in ammonia‐treated cells only and the effect of cANP<jats:sub>(4–23)</jats:sub> was decreased when the NADPH oxidase‐regulatory protein G<jats:sub>iα‐2</jats:sub> was blocked with a specific anti‐G<jats:sub>iα‐2</jats:sub> antibody. Although in contrast to ANP, cANP<jats:sub>(4–23)</jats:sub> did not elevate the cGMP content in control astrocytes, it decreased cAMP content and reduced the expression of G<jats:sub>iα‐2</jats:sub>, the NADPH oxidase‐regulatory protein. The results show the presence of functional NPR‐C in astrocytes, activation of which (i) attenuates basal ROS production, and (ii) prevents excessive accumulation of the toxic ROS species, •O<jats:sub>2</jats:sub><jats:sup>−</jats:sup> by ammonia. Ammonia, ANP and cANP<jats:sub>(4–23)</jats:sub> added separately, each stimulated formation of NO<jats:sub>x</jats:sub> (nitrates + nitrites) which was associated with up‐regulation of the activity [cANP<jats:sub>(4–23)</jats:sub>] or/and expression (ammonia) of the endothelial isoform of nitric oxide synthase. However, the ammonia‐induced increase of NO<jats:sub>x</jats:sub> was not augmented by co‐addition of ANP, and was reduced to the control level by co‐addition of cANP<jats:sub>(4–23)</jats:sub>, indicating that activation of NPR‐C may also reduce nitrosative stress. Future hepatic encephalopathy therapy might include the use of cANP<jats:sub>(4–23)</jats:sub> or other NPR‐C agonists to control oxidative/nitrosative stress induced by ammonia.</jats:p></jats:sec> |
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author | Skowrońska, Marta, Zielińska, Magdalena, Albrecht, Jan |
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spelling | Skowrońska, Marta Zielińska, Magdalena Albrecht, Jan 0022-3042 1471-4159 Wiley Cellular and Molecular Neuroscience Biochemistry http://dx.doi.org/10.1111/j.1471-4159.2010.07008.x <jats:sec><jats:label /><jats:p> <jats:italic>J. Neurochem.</jats:italic> (2010) <jats:bold>115</jats:bold>, 1068–1076.</jats:p></jats:sec><jats:sec><jats:title>Abstract</jats:title><jats:p>Oxidative and nitrosative stress contribute to ammonia‐induced astrocytic dysfunction in hepatic encephalopathy. Treatment of cultured astrocytes with 5 mmol/L ammonium chloride (‘ammonia’) increased the production of reactive oxygen species (ROS), including the toxic NADPH oxidase reaction product, •O<jats:sub>2</jats:sub><jats:sup>−</jats:sup>. Atrial natriuretic peptide (ANP), natriuretic peptide C and a selective natriuretic peptide receptor (NPR)‐C ligand, cANP<jats:sub>(4–23),</jats:sub> each decreased the total ROS content both in control cells and cells treated with ammonia. However, attenuation of •O<jats:sub>2</jats:sub><jats:sup>−</jats:sup> accumulation by ANP and cANP<jats:sub>(4–23),</jats:sub> was observed in ammonia‐treated cells only and the effect of cANP<jats:sub>(4–23)</jats:sub> was decreased when the NADPH oxidase‐regulatory protein G<jats:sub>iα‐2</jats:sub> was blocked with a specific anti‐G<jats:sub>iα‐2</jats:sub> antibody. Although in contrast to ANP, cANP<jats:sub>(4–23)</jats:sub> did not elevate the cGMP content in control astrocytes, it decreased cAMP content and reduced the expression of G<jats:sub>iα‐2</jats:sub>, the NADPH oxidase‐regulatory protein. The results show the presence of functional NPR‐C in astrocytes, activation of which (i) attenuates basal ROS production, and (ii) prevents excessive accumulation of the toxic ROS species, •O<jats:sub>2</jats:sub><jats:sup>−</jats:sup> by ammonia. Ammonia, ANP and cANP<jats:sub>(4–23)</jats:sub> added separately, each stimulated formation of NO<jats:sub>x</jats:sub> (nitrates + nitrites) which was associated with up‐regulation of the activity [cANP<jats:sub>(4–23)</jats:sub>] or/and expression (ammonia) of the endothelial isoform of nitric oxide synthase. However, the ammonia‐induced increase of NO<jats:sub>x</jats:sub> was not augmented by co‐addition of ANP, and was reduced to the control level by co‐addition of cANP<jats:sub>(4–23)</jats:sub>, indicating that activation of NPR‐C may also reduce nitrosative stress. Future hepatic encephalopathy therapy might include the use of cANP<jats:sub>(4–23)</jats:sub> or other NPR‐C agonists to control oxidative/nitrosative stress induced by ammonia.</jats:p></jats:sec> Stimulation of natriuretic peptide receptor C attenuates accumulation of reactive oxygen species and nitric oxide synthesis in ammonia‐treated astrocytes Journal of Neurochemistry |
spellingShingle | Skowrońska, Marta, Zielińska, Magdalena, Albrecht, Jan, Journal of Neurochemistry, Stimulation of natriuretic peptide receptor C attenuates accumulation of reactive oxygen species and nitric oxide synthesis in ammonia‐treated astrocytes, Cellular and Molecular Neuroscience, Biochemistry |
title | Stimulation of natriuretic peptide receptor C attenuates accumulation of reactive oxygen species and nitric oxide synthesis in ammonia‐treated astrocytes |
title_full | Stimulation of natriuretic peptide receptor C attenuates accumulation of reactive oxygen species and nitric oxide synthesis in ammonia‐treated astrocytes |
title_fullStr | Stimulation of natriuretic peptide receptor C attenuates accumulation of reactive oxygen species and nitric oxide synthesis in ammonia‐treated astrocytes |
title_full_unstemmed | Stimulation of natriuretic peptide receptor C attenuates accumulation of reactive oxygen species and nitric oxide synthesis in ammonia‐treated astrocytes |
title_short | Stimulation of natriuretic peptide receptor C attenuates accumulation of reactive oxygen species and nitric oxide synthesis in ammonia‐treated astrocytes |
title_sort | stimulation of natriuretic peptide receptor c attenuates accumulation of reactive oxygen species and nitric oxide synthesis in ammonia‐treated astrocytes |
title_unstemmed | Stimulation of natriuretic peptide receptor C attenuates accumulation of reactive oxygen species and nitric oxide synthesis in ammonia‐treated astrocytes |
topic | Cellular and Molecular Neuroscience, Biochemistry |
url | http://dx.doi.org/10.1111/j.1471-4159.2010.07008.x |