author_facet Skowrońska, Marta
Zielińska, Magdalena
Albrecht, Jan
Skowrońska, Marta
Zielińska, Magdalena
Albrecht, Jan
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
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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
author_facet Skowrońska, Marta, Zielińska, Magdalena, Albrecht, Jan, Skowrońska, Marta, Zielińska, Magdalena, Albrecht, Jan
author_sort skowrońska, marta
container_issue 4
container_start_page 1068
container_title Journal of Neurochemistry
container_volume 115
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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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