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Notch1 Signaling Activation Contributes to Adult Hippocampal Neurogenesis Following Traumatic Brain Injury

BACKGROUND: Neural stem cells are reported to exist in the hippocampus of adult mammals and are important sources of neurons for repair. The Notch1 signaling pathway is considered as one of the important regulators of neural stem cells, but its role in adult brains is unclear. We aimed to describe t...

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Autores principales: Tu, Ming, Zhu, Penglei, Hu, Shaobo, Wang, Wei, Su, Zhipeng, Guan, Jiaqing, Sun, Chongran, Zheng, Weiming
Formato: Online Artículo Texto
Lenguaje:English
Publicado: International Scientific Literature, Inc. 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5703017/
https://www.ncbi.nlm.nih.gov/pubmed/29150595
http://dx.doi.org/10.12659/MSM.907160
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author Tu, Ming
Zhu, Penglei
Hu, Shaobo
Wang, Wei
Su, Zhipeng
Guan, Jiaqing
Sun, Chongran
Zheng, Weiming
author_facet Tu, Ming
Zhu, Penglei
Hu, Shaobo
Wang, Wei
Su, Zhipeng
Guan, Jiaqing
Sun, Chongran
Zheng, Weiming
author_sort Tu, Ming
collection PubMed
description BACKGROUND: Neural stem cells are reported to exist in the hippocampus of adult mammals and are important sources of neurons for repair. The Notch1 signaling pathway is considered as one of the important regulators of neural stem cells, but its role in adult brains is unclear. We aimed to describe the role of Notch1 signaling in the adult rat hippocampus after traumatic brain injury. MATERIAL/METHODS: The model rats were randomly divided into 4 groups as follows: sham, sham-TBI, sham-Ad-TBI, and NICD-Ad-TBI. We used adenovirus-mediated gene transfection to upregulate endogenous NICD in vivo. Firstly, a TBI rat model was constructed with lateral fluid percussion. Then, the hippocampus was collected to detect the expression of Notch1 markers and stem cell markers (DCX) by Western blot analysis, immunohistochemistry, and immunofluorescence. The prognosis after TBI treatment was evaluated by the Morris Water Maze test. RESULTS: First, we found the expression of NICD in vivo was significantly increased by adenovirus-mediated gene transfection as assessed by Notch1 immunofluorescence and Western blot analysis. Second, enhancing NICD stimulated the regeneration of neural stem cells in the DG of the adult rat brain following traumatic brain injury, as evaluated by DCX and NeuN double-staining. Furthermore, Notch1 signaling activation can promote behavioral improvement after traumatic brain injury, including spatial learning and memory capacity. CONCLUSIONS: Our findings suggest that targeted regulation of Notch1 signaling may have a useful effect on stem cell transformation. Notch1 signaling may have a potential brain-protection effect, which may result from neurogenesis.
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spelling pubmed-57030172017-11-29 Notch1 Signaling Activation Contributes to Adult Hippocampal Neurogenesis Following Traumatic Brain Injury Tu, Ming Zhu, Penglei Hu, Shaobo Wang, Wei Su, Zhipeng Guan, Jiaqing Sun, Chongran Zheng, Weiming Med Sci Monit Animal Study BACKGROUND: Neural stem cells are reported to exist in the hippocampus of adult mammals and are important sources of neurons for repair. The Notch1 signaling pathway is considered as one of the important regulators of neural stem cells, but its role in adult brains is unclear. We aimed to describe the role of Notch1 signaling in the adult rat hippocampus after traumatic brain injury. MATERIAL/METHODS: The model rats were randomly divided into 4 groups as follows: sham, sham-TBI, sham-Ad-TBI, and NICD-Ad-TBI. We used adenovirus-mediated gene transfection to upregulate endogenous NICD in vivo. Firstly, a TBI rat model was constructed with lateral fluid percussion. Then, the hippocampus was collected to detect the expression of Notch1 markers and stem cell markers (DCX) by Western blot analysis, immunohistochemistry, and immunofluorescence. The prognosis after TBI treatment was evaluated by the Morris Water Maze test. RESULTS: First, we found the expression of NICD in vivo was significantly increased by adenovirus-mediated gene transfection as assessed by Notch1 immunofluorescence and Western blot analysis. Second, enhancing NICD stimulated the regeneration of neural stem cells in the DG of the adult rat brain following traumatic brain injury, as evaluated by DCX and NeuN double-staining. Furthermore, Notch1 signaling activation can promote behavioral improvement after traumatic brain injury, including spatial learning and memory capacity. CONCLUSIONS: Our findings suggest that targeted regulation of Notch1 signaling may have a useful effect on stem cell transformation. Notch1 signaling may have a potential brain-protection effect, which may result from neurogenesis. International Scientific Literature, Inc. 2017-11-18 /pmc/articles/PMC5703017/ /pubmed/29150595 http://dx.doi.org/10.12659/MSM.907160 Text en © Med Sci Monit, 2017 This work is licensed under Creative Common Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0 (https://creativecommons.org/licenses/by-nc-nd/4.0/) )
spellingShingle Animal Study
Tu, Ming
Zhu, Penglei
Hu, Shaobo
Wang, Wei
Su, Zhipeng
Guan, Jiaqing
Sun, Chongran
Zheng, Weiming
Notch1 Signaling Activation Contributes to Adult Hippocampal Neurogenesis Following Traumatic Brain Injury
title Notch1 Signaling Activation Contributes to Adult Hippocampal Neurogenesis Following Traumatic Brain Injury
title_full Notch1 Signaling Activation Contributes to Adult Hippocampal Neurogenesis Following Traumatic Brain Injury
title_fullStr Notch1 Signaling Activation Contributes to Adult Hippocampal Neurogenesis Following Traumatic Brain Injury
title_full_unstemmed Notch1 Signaling Activation Contributes to Adult Hippocampal Neurogenesis Following Traumatic Brain Injury
title_short Notch1 Signaling Activation Contributes to Adult Hippocampal Neurogenesis Following Traumatic Brain Injury
title_sort notch1 signaling activation contributes to adult hippocampal neurogenesis following traumatic brain injury
topic Animal Study
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5703017/
https://www.ncbi.nlm.nih.gov/pubmed/29150595
http://dx.doi.org/10.12659/MSM.907160
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