Adult neurogenesis transiently generates oxidative stress.

An increasing body of evidence suggests that alterations in neurogenesis and oxidative stress are associated with a wide variety of CNS diseases, including Alzheimer's disease, schizophrenia and Parkinson's disease, as well as routine loss of function accompanying aging. Interestingly, the...

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Autores principales:	Noah M Walton, Rick Shin, Katsunori Tajinda, Carrie L Heusner, Jeffrey H Kogan, Shinichi Miyake, Qian Chen, Kouichi Tamura, Mitsuyuki Matsumoto
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2012
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/ea47c047cca740fe9aee274e17271dea
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spelling	oai:doaj.org-article:ea47c047cca740fe9aee274e17271dea2021-11-18T07:20:14ZAdult neurogenesis transiently generates oxidative stress.1932-620310.1371/journal.pone.0035264https://doaj.org/article/ea47c047cca740fe9aee274e17271dea2012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22558133/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203An increasing body of evidence suggests that alterations in neurogenesis and oxidative stress are associated with a wide variety of CNS diseases, including Alzheimer's disease, schizophrenia and Parkinson's disease, as well as routine loss of function accompanying aging. Interestingly, the association between neurogenesis and the production of reactive oxidative species (ROS) remains largely unexamined. The adult CNS harbors two regions of persistent lifelong neurogenesis: the subventricular zone and the dentate gyrus (DG). These regions contain populations of quiescent neural stem cells (NSCs) that generate mature progeny via rapidly-dividing progenitor cells. We hypothesized that the energetic demands of highly proliferative progenitors generates localized oxidative stress that contributes to ROS-mediated damage within the neuropoietic microenvironment. In vivo examination of germinal niches in adult rodents revealed increases in oxidized DNA and lipid markers, particularly in the subgranular zone (SGZ) of the dentate gyrus. To further pinpoint the cell types responsible for oxidative stress, we employed an in vitro cell culture model allowing for the synchronous terminal differentiation of primary hippocampal NSCs. Inducing differentiation in primary NSCs resulted in an immediate increase in total mitochondria number and overall ROS production, suggesting oxidative stress is generated during a transient window of elevated neurogenesis accompanying normal neurogenesis. To confirm these findings in vivo, we identified a set of oxidation-responsive genes, which respond to antioxidant administration and are significantly elevated in genetic- and exercise-induced model of hyperactive hippocampal neurogenesis. While no direct evidence exists coupling neurogenesis-associated stress to CNS disease, our data suggest that oxidative stress is produced as a result of routine adult neurogenesis.Noah M WaltonRick ShinKatsunori TajindaCarrie L HeusnerJeffrey H KoganShinichi MiyakeQian ChenKouichi TamuraMitsuyuki MatsumotoPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 4, p e35264 (2012)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Noah M Walton Rick Shin Katsunori Tajinda Carrie L Heusner Jeffrey H Kogan Shinichi Miyake Qian Chen Kouichi Tamura Mitsuyuki Matsumoto Adult neurogenesis transiently generates oxidative stress.
description	An increasing body of evidence suggests that alterations in neurogenesis and oxidative stress are associated with a wide variety of CNS diseases, including Alzheimer's disease, schizophrenia and Parkinson's disease, as well as routine loss of function accompanying aging. Interestingly, the association between neurogenesis and the production of reactive oxidative species (ROS) remains largely unexamined. The adult CNS harbors two regions of persistent lifelong neurogenesis: the subventricular zone and the dentate gyrus (DG). These regions contain populations of quiescent neural stem cells (NSCs) that generate mature progeny via rapidly-dividing progenitor cells. We hypothesized that the energetic demands of highly proliferative progenitors generates localized oxidative stress that contributes to ROS-mediated damage within the neuropoietic microenvironment. In vivo examination of germinal niches in adult rodents revealed increases in oxidized DNA and lipid markers, particularly in the subgranular zone (SGZ) of the dentate gyrus. To further pinpoint the cell types responsible for oxidative stress, we employed an in vitro cell culture model allowing for the synchronous terminal differentiation of primary hippocampal NSCs. Inducing differentiation in primary NSCs resulted in an immediate increase in total mitochondria number and overall ROS production, suggesting oxidative stress is generated during a transient window of elevated neurogenesis accompanying normal neurogenesis. To confirm these findings in vivo, we identified a set of oxidation-responsive genes, which respond to antioxidant administration and are significantly elevated in genetic- and exercise-induced model of hyperactive hippocampal neurogenesis. While no direct evidence exists coupling neurogenesis-associated stress to CNS disease, our data suggest that oxidative stress is produced as a result of routine adult neurogenesis.
format	article
author	Noah M Walton Rick Shin Katsunori Tajinda Carrie L Heusner Jeffrey H Kogan Shinichi Miyake Qian Chen Kouichi Tamura Mitsuyuki Matsumoto
author_facet	Noah M Walton Rick Shin Katsunori Tajinda Carrie L Heusner Jeffrey H Kogan Shinichi Miyake Qian Chen Kouichi Tamura Mitsuyuki Matsumoto
author_sort	Noah M Walton
title	Adult neurogenesis transiently generates oxidative stress.
title_short	Adult neurogenesis transiently generates oxidative stress.
title_full	Adult neurogenesis transiently generates oxidative stress.
title_fullStr	Adult neurogenesis transiently generates oxidative stress.
title_full_unstemmed	Adult neurogenesis transiently generates oxidative stress.
title_sort	adult neurogenesis transiently generates oxidative stress.
publisher	Public Library of Science (PLoS)
publishDate	2012
url	https://doaj.org/article/ea47c047cca740fe9aee274e17271dea
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Adult neurogenesis transiently generates oxidative stress.

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