Astrocyte Depletion Impairs Redox Homeostasis and Triggers Neuronal Loss in the Adult CNS

Although the importance of reactive astrocytes during CNS pathology is well established, the function of astroglia in adult CNS homeostasis is less well understood. With the use of conditional, astrocyte-restricted protein synthesis termination, we found that selective paralysis of GFAP+ astrocytes...

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Published in:	Cell reports (Cambridge) Vol. 12; no. 9; pp. 1377 - 1384
Main Authors:	Schreiner, Bettina, Romanelli, Elisa, Liberski, Pawel, Ingold-Heppner, Barbara, Sobottka-Brillout, Bettina, Hartwig, Tom, Chandrasekar, Vijay, Johannssen, Helge, Zeilhofer, Hanns Ulrich, Aguzzi, Adriano, Heppner, Frank, Kerschensteiner, Martin, Becher, Burkhard
Format:	Journal Article
Language:	English
Published:	United States Elsevier Inc 01.09.2015 Elsevier
Subjects:	Animals Antioxidants - pharmacology Astrocytes - metabolism Brain - cytology Brain - drug effects Brain - growth & development Brain - metabolism Cell Death Glial Fibrillary Acidic Protein - genetics Glial Fibrillary Acidic Protein - metabolism Mice Motor Neurons - metabolism Oxidative Stress Reactive Nitrogen Species - metabolism Reactive Oxygen Species - metabolism
ISSN:	2211-1247, 2211-1247
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Abstract	Although the importance of reactive astrocytes during CNS pathology is well established, the function of astroglia in adult CNS homeostasis is less well understood. With the use of conditional, astrocyte-restricted protein synthesis termination, we found that selective paralysis of GFAP+ astrocytes in vivo led to rapid neuronal cell loss and severe motor deficits. This occurred while structural astroglial support still persisted and in the absence of any major microvascular damage. Whereas loss of astrocyte function did lead to microglial activation, this had no impact on the neuronal loss and clinical decline. Neuronal injury was caused by oxidative stress resulting from the reduced redox scavenging capability of dysfunctional astrocytes and could be prevented by the in vivo treatment with scavengers of reactive oxygen and nitrogen species (ROS/RNS). Our results suggest that the subpopulation of GFAP+ astrocytes maintain neuronal health by controlling redox homeostasis in the adult CNS. [Display omitted] •When adult GFAP+ astrocytes are depleted in vivo, motor skills are severely impaired•Neuronal loss occurs, whereas astroglial structural support still persists•Astroglial dysfunction disrupts CNS redox homeostasis, independent of microgliosis•Neutralization of ROS/RNS protects from neuronal injury Schreiner et al. examine the functional contribution of astrocytes to tissue homeostasis in the adult CNS and identify the redox-scavenging capacity of GFAP+ astrocytes as a key factor for neuronal health in vivo. The importance of the metabolic integrity of the glia-neuron interface highlights potential therapies for the treatment of neurodegenerative diseases.
AbstractList	Although the importance of reactive astrocytes during CNS pathology is well established, the function of astroglia in adult CNS homeostasis is less well understood. With the use of conditional, astrocyte-restricted protein synthesis termination, we found that selective paralysis of GFAP(+) astrocytes in vivo led to rapid neuronal cell loss and severe motor deficits. This occurred while structural astroglial support still persisted and in the absence of any major microvascular damage. Whereas loss of astrocyte function did lead to microglial activation, this had no impact on the neuronal loss and clinical decline. Neuronal injury was caused by oxidative stress resulting from the reduced redox scavenging capability of dysfunctional astrocytes and could be prevented by the in vivo treatment with scavengers of reactive oxygen and nitrogen species (ROS/RNS). Our results suggest that the subpopulation of GFAP(+) astrocytes maintain neuronal health by controlling redox homeostasis in the adult CNS.Although the importance of reactive astrocytes during CNS pathology is well established, the function of astroglia in adult CNS homeostasis is less well understood. With the use of conditional, astrocyte-restricted protein synthesis termination, we found that selective paralysis of GFAP(+) astrocytes in vivo led to rapid neuronal cell loss and severe motor deficits. This occurred while structural astroglial support still persisted and in the absence of any major microvascular damage. Whereas loss of astrocyte function did lead to microglial activation, this had no impact on the neuronal loss and clinical decline. Neuronal injury was caused by oxidative stress resulting from the reduced redox scavenging capability of dysfunctional astrocytes and could be prevented by the in vivo treatment with scavengers of reactive oxygen and nitrogen species (ROS/RNS). Our results suggest that the subpopulation of GFAP(+) astrocytes maintain neuronal health by controlling redox homeostasis in the adult CNS. Although the importance of reactive astrocytes during CNS pathology is well established, the function of astroglia in adult CNS homeostasis is less well understood. With the use of conditional, astrocyte-restricted protein synthesis termination, we found that selective paralysis of GFAP+ astrocytes in vivo led to rapid neuronal cell loss and severe motor deficits. This occurred while structural astroglial support still persisted and in the absence of any major microvascular damage. Whereas loss of astrocyte function did lead to microglial activation, this had no impact on the neuronal loss and clinical decline. Neuronal injury was caused by oxidative stress resulting from the reduced redox scavenging capability of dysfunctional astrocytes and could be prevented by the in vivo treatment with scavengers of reactive oxygen and nitrogen species (ROS/RNS). Our results suggest that the subpopulation of GFAP+ astrocytes maintain neuronal health by controlling redox homeostasis in the adult CNS. Although the importance of reactive astrocytes during CNS pathology is well established, the function of astroglia in adult CNS homeostasis is less well understood. With the use of conditional, astrocyte-restricted protein synthesis termination, we found that selective paralysis of GFAP+ astrocytes in vivo led to rapid neuronal cell loss and severe motor deficits. This occurred while structural astroglial support still persisted and in the absence of any major microvascular damage. Whereas loss of astrocyte function did lead to microglial activation, this had no impact on the neuronal loss and clinical decline. Neuronal injury was caused by oxidative stress resulting from the reduced redox scavenging capability of dysfunctional astrocytes and could be prevented by the in vivo treatment with scavengers of reactive oxygen and nitrogen species (ROS/RNS). Our results suggest that the subpopulation of GFAP+ astrocytes maintain neuronal health by controlling redox homeostasis in the adult CNS. [Display omitted] •When adult GFAP+ astrocytes are depleted in vivo, motor skills are severely impaired•Neuronal loss occurs, whereas astroglial structural support still persists•Astroglial dysfunction disrupts CNS redox homeostasis, independent of microgliosis•Neutralization of ROS/RNS protects from neuronal injury Schreiner et al. examine the functional contribution of astrocytes to tissue homeostasis in the adult CNS and identify the redox-scavenging capacity of GFAP+ astrocytes as a key factor for neuronal health in vivo. The importance of the metabolic integrity of the glia-neuron interface highlights potential therapies for the treatment of neurodegenerative diseases. Although the importance of reactive astrocytes during CNS pathology is well established, the function of astroglia in adult CNS homeostasis is less well understood. With the use of conditional, astrocyte-restricted protein synthesis termination, we found that selective paralysis of GFAP(+) astrocytes in vivo led to rapid neuronal cell loss and severe motor deficits. This occurred while structural astroglial support still persisted and in the absence of any major microvascular damage. Whereas loss of astrocyte function did lead to microglial activation, this had no impact on the neuronal loss and clinical decline. Neuronal injury was caused by oxidative stress resulting from the reduced redox scavenging capability of dysfunctional astrocytes and could be prevented by the in vivo treatment with scavengers of reactive oxygen and nitrogen species (ROS/RNS). Our results suggest that the subpopulation of GFAP(+) astrocytes maintain neuronal health by controlling redox homeostasis in the adult CNS.
Author	Sobottka-Brillout, Bettina Johannssen, Helge Schreiner, Bettina Aguzzi, Adriano Hartwig, Tom Heppner, Frank Becher, Burkhard Kerschensteiner, Martin Ingold-Heppner, Barbara Romanelli, Elisa Zeilhofer, Hanns Ulrich Liberski, Pawel Chandrasekar, Vijay
Author_xml	– sequence: 1 givenname: Bettina surname: Schreiner fullname: Schreiner, Bettina organization: Institute of Experimental Immunology, University of Zurich, 8057 Zurich, Switzerland – sequence: 2 givenname: Elisa surname: Romanelli fullname: Romanelli, Elisa organization: Institute of Clinical Neuroimmunology, Ludwig-Maximilians Universität München, 81377 Munich, Germany – sequence: 3 givenname: Pawel surname: Liberski fullname: Liberski, Pawel organization: Department of Molecular Pathology and Neuropathology, Medical University of Lodz, 92-101 Lodz, Poland – sequence: 4 givenname: Barbara surname: Ingold-Heppner fullname: Ingold-Heppner, Barbara organization: Department of Pathology, Charité-Universitätsmedizin Berlin, 10117 Berlin, Germany – sequence: 5 givenname: Bettina surname: Sobottka-Brillout fullname: Sobottka-Brillout, Bettina organization: Institute of Experimental Immunology, University of Zurich, 8057 Zurich, Switzerland – sequence: 6 givenname: Tom surname: Hartwig fullname: Hartwig, Tom organization: Institute of Experimental Immunology, University of Zurich, 8057 Zurich, Switzerland – sequence: 7 givenname: Vijay surname: Chandrasekar fullname: Chandrasekar, Vijay organization: Institute of Neuropathology, University Hospital Zurich, 8091 Zurich, Switzerland – sequence: 8 givenname: Helge surname: Johannssen fullname: Johannssen, Helge organization: Institute of Pharmacology and Toxicology, University of Zurich, 8057 Zurich, Switzerland – sequence: 9 givenname: Hanns Ulrich surname: Zeilhofer fullname: Zeilhofer, Hanns Ulrich organization: Institute of Pharmacology and Toxicology, University of Zurich, 8057 Zurich, Switzerland – sequence: 10 givenname: Adriano surname: Aguzzi fullname: Aguzzi, Adriano organization: Institute of Neuropathology, University Hospital Zurich, 8091 Zurich, Switzerland – sequence: 11 givenname: Frank surname: Heppner fullname: Heppner, Frank organization: Department of Neuropathology, Charité-Universitätsmedizin Berlin, 10117 Berlin, Germany – sequence: 12 givenname: Martin surname: Kerschensteiner fullname: Kerschensteiner, Martin organization: Institute of Clinical Neuroimmunology, Ludwig-Maximilians Universität München, 81377 Munich, Germany – sequence: 13 givenname: Burkhard surname: Becher fullname: Becher, Burkhard email: becher@immunology.uzh.ch organization: Institute of Experimental Immunology, University of Zurich, 8057 Zurich, Switzerland
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Snippet	Although the importance of reactive astrocytes during CNS pathology is well established, the function of astroglia in adult CNS homeostasis is less well...
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SubjectTerms	Animals Antioxidants - pharmacology Astrocytes - metabolism Brain - cytology Brain - drug effects Brain - growth & development Brain - metabolism Cell Death Glial Fibrillary Acidic Protein - genetics Glial Fibrillary Acidic Protein - metabolism Mice Motor Neurons - metabolism Oxidative Stress Reactive Nitrogen Species - metabolism Reactive Oxygen Species - metabolism
Title	Astrocyte Depletion Impairs Redox Homeostasis and Triggers Neuronal Loss in the Adult CNS
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