Appearance of neural stem cells around the damaged area following traumatic brain injury in aged rats

We have previously reported free radical production after traumatic brain injury (TBI), which induces neural stem cell (NSC) degeneration and death. However, the effects of aging on NSC proliferation around the damaged area following TBI have not been investigated. Therefore, in this study, we used...

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Veröffentlicht in:Journal of Neural Transmission 2013-03, Vol.120 (3), p.361-374
Hauptverfasser: Itoh, Tatsuki, Imano, Motohiro, Nishida, Shozo, Tsubaki, Masahiro, Nakayama, Takashi, Mizuguchi, Nobuyuki, Yamanaka, Shigeaki, Tabuchi, Masaki, Munakata, Hiroshi, Hashimoto, Shigeo, Ito, Akihiko, Satou, Takao
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container_title Journal of Neural Transmission
container_volume 120
creator Itoh, Tatsuki
Imano, Motohiro
Nishida, Shozo
Tsubaki, Masahiro
Nakayama, Takashi
Mizuguchi, Nobuyuki
Yamanaka, Shigeaki
Tabuchi, Masaki
Munakata, Hiroshi
Hashimoto, Shigeo
Ito, Akihiko
Satou, Takao
description We have previously reported free radical production after traumatic brain injury (TBI), which induces neural stem cell (NSC) degeneration and death. However, the effects of aging on NSC proliferation around the damaged area following TBI have not been investigated. Therefore, in this study, we used 10-week (young group) and 24-month-old (aged group) rat TBI models to investigate the effects of aging on NSC proliferation around damaged tissue using immunohistochemical and ex vivo techniques. Young and aged rats received TBI. At 1, 3 and 7 days after TBI, immunohistochemical and lipid peroxidation studies were performed. Immunohistochemistry revealed that the number of nestin-positive cells around the damaged area after TBI in the aged group decreased significantly when compared with those in the young group ( P  
doi_str_mv 10.1007/s00702-012-0895-7
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However, the effects of aging on NSC proliferation around the damaged area following TBI have not been investigated. Therefore, in this study, we used 10-week (young group) and 24-month-old (aged group) rat TBI models to investigate the effects of aging on NSC proliferation around damaged tissue using immunohistochemical and ex vivo techniques. Young and aged rats received TBI. At 1, 3 and 7 days after TBI, immunohistochemical and lipid peroxidation studies were performed. Immunohistochemistry revealed that the number of nestin-positive cells around the damaged area after TBI in the aged group decreased significantly when compared with those in the young group ( P  &lt; 0.01). However, the number of 8-hydroxy-2′-deoxyguanosine-, 4-hydroxy-2-nonenal- and single-stranded DNA (ssDNA)-positive cells and the level of peroxidation around the damaged area after TBI significantly increased in the aged group, compared with those in the young group ( P  &lt; 0.01). Furthermore, almost all ssDNA-positive cells in young and aged groups co-localized with NeuN and nestin staining. Ex vivo studies revealed that neurospheres, which differentiated into neurons and glia in culture, could only be isolated from injured brain tissue in young and aged groups at 3 days after TBI. 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However, the effects of aging on NSC proliferation around the damaged area following TBI have not been investigated. Therefore, in this study, we used 10-week (young group) and 24-month-old (aged group) rat TBI models to investigate the effects of aging on NSC proliferation around damaged tissue using immunohistochemical and ex vivo techniques. Young and aged rats received TBI. At 1, 3 and 7 days after TBI, immunohistochemical and lipid peroxidation studies were performed. Immunohistochemistry revealed that the number of nestin-positive cells around the damaged area after TBI in the aged group decreased significantly when compared with those in the young group ( P  &lt; 0.01). However, the number of 8-hydroxy-2′-deoxyguanosine-, 4-hydroxy-2-nonenal- and single-stranded DNA (ssDNA)-positive cells and the level of peroxidation around the damaged area after TBI significantly increased in the aged group, compared with those in the young group ( P  &lt; 0.01). Furthermore, almost all ssDNA-positive cells in young and aged groups co-localized with NeuN and nestin staining. Ex vivo studies revealed that neurospheres, which differentiated into neurons and glia in culture, could only be isolated from injured brain tissue in young and aged groups at 3 days after TBI. These results indicate that, although there were fewer NSCs that have the potential to differentiate into neurons and glia, these NSCs escaped free radical-induced degeneration around the damaged area after TBI in the aged rat brain.</abstract><cop>Vienna</cop><pub>Springer Vienna</pub><pmid>22955958</pmid><doi>10.1007/s00702-012-0895-7</doi><tpages>14</tpages></addata></record>
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subjects Aging
Aldehydes - analysis
Animals
Brain Injuries - metabolism
Brain Injuries - pathology
Cell culture
Cell Differentiation - physiology
Deoxyguanosine - analogs & derivatives
Deoxyguanosine - analysis
Deoxyguanosine - biosynthesis
Disease Models, Animal
DNA
DNA, Single-Stranded - analysis
Fluorescent Antibody Technique
Free radicals
Glia
Immunohistochemistry
Intermediate Filament Proteins - analysis
Intermediate Filament Proteins - biosynthesis
Lipid peroxidation
Lipid Peroxidation - physiology
Male
Medicine
Medicine & Public Health
Nerve Tissue Proteins - analysis
Nerve Tissue Proteins - biosynthesis
Nestin
Neural stem cells
Neural Stem Cells - cytology
Neural Stem Cells - metabolism
Neurodegeneration
Neurology
Neurons
Neurosciences
neurospheres
Peroxidation
Psychiatry
Rats
Rats, Wistar
Translational Neurosciences - Original Article
Traumatic brain injury
title Appearance of neural stem cells around the damaged area following traumatic brain injury in aged rats
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