Traumatic Brain Injury Stimulates Neural Stem Cell Proliferation via Mammalian Target of Rapamycin Signaling Pathway Activation

Wang, Xiaoting; Seekaew, Pich; Gao, Xiang; Chen, Jinhui

doi:10.1523/eneuro.0162-16.2016

Cited by 25 publications

(19 citation statements)

References 83 publications

(138 reference statements)

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“…There are several factors contributing to the proliferation of endogenous neural stem cells, as the enhanced level of oxidative stress and cytokines in the brain reduces the proliferation of neural stem cells. The literature reveals that treatment with zerumbone reduces the level of inflammatory cytokines and oxidative stress [4,18]. Results of our study suggest that zerumbone ameliorates the altered level of cytokines and parameters of oxidative stress in the brain tissue compared to the VD rats in a dose dependent manner.…”

Section: Discussionsupporting

confidence: 52%

Zerumbone promotes proliferation of endogenous neural stem cells in vascular dementia by regulating Notch signalling

Sun

et al. 2019

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Introduction: Present investigation determines the effect of zerumbone on the proliferation of stem cells in vascular dementia (VD) rats. Material and methods: Vascular dementia was induced by cerebral ischemia and reperfusion through non-invasive clamp. Rats were treated with zerumbone 50 mg/kg and 100 mg/kg intraperitoneally 30 min for four weeks after the surgery. Cognitive functions are determined by the Morris water maze (MWM) test and neurological function score in VD rats. Moreover mediators of inflammation and parameters of oxidative stress were estimated in the brain tissue homogenate of ischemia-induced vascular dementia rats. The expression of proteins and mRNA expressions were determined by western blot assay and RT-PCR methods. Moreover histopathological changes were observed by H&E staining on the brain tissue of vascular dementia rats. Results: There was a significant reduction in the cognitive function and neurological score in the zerumbone-treated group compared to the VD group of rats. Data of the study reveal that treatment with zerumbone attenuates the altered level of cytokines and markers of oxidative stress parameters in the brain tissue of VD rats. The expression of NICD, Hes-1 and Nestin proteins was significantly (p < 0.01) reduced in the brain tissue of the zerumbone-treated group compared to the VD group of rats. There was a significant reduction in the mRNA expression of Notch-1 and Hes-1 in the brain tissue of the zerumbone-treated group compared to the VD group of rats. Conclusions: This study concludes that treatment with zerumbone protects the neuronal injury and ameliorates the cognitive function by stimulating the proliferation of endogenous neural stem cells. Moreover proliferation of neural stem cells was stimulated in zerumbone-treated rats by regulating the Notch signalling.

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Section: Discussionsupporting

confidence: 52%

Zerumbone promotes proliferation of endogenous neural stem cells in vascular dementia by regulating Notch signalling

Sun

et al. 2019

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“…In literature, Xiaoting et al . (2016) [65] suggested the role of mTOR in neural-stem-cell (NSC) proliferation after injury. After TBI, extracellular signal-regulated kinase (ERK) level is increased, whereas, the PI3K level is decreased which results in the activation of various kinases like (protein kinase B) AKT [66].…”

Section: Tbi Altered Normal Brain Signaling Pathwaysmentioning

confidence: 99%

Traumatic Brain Injury Altered Normal Brain Signaling Pathways: Implications for Novel Therapeutics Approaches

Rana

Singh

Sharma

et al. 2019

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Traumatic brain injury (TBI) is the main reason of lifelong disability and casualty worldwide. In the United state alone, 1.7 million traumatic events occur yearly, out of which 50,000 results in deaths. Injury to the brain could alter various biological signaling pathways such as excitotoxicity, ionic imbalance, oxidative stress, inflammation, and apoptosis which can result in various neurological disorders such as Psychosis, Depression, Alzheimer disease, Parkinson disease, etc. In literature, various reports have indicated the alteration of these pathways after traumatic brain injury but the exact mechanism is still unclear. Thus, in the first part of this article, we have tried to summarize TBI as a modulator of various neuronal signaling pathways. Currently, very few drugs are available in the market for the treatment of TBI and these drugs only provide the supportive care. Thus, in the second part of the article, based on TBI altered signaling pathways, we have tried to find out potential targets and promising therapeutic approaches in the treatment of TBI.

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“…To assess newly-generated neurons and proliferated cells in Dentate Gyrus (DG), mice received BrdU (50 mg/kg, i.p. dissolved in saline) every day for seven days after TBI [49]. BrdU incorporation into cell nuclei was assessed by immunohistochemistry.…”

Section: Bromodeoxyuridine (Brdu) Treatmentmentioning

confidence: 99%

Formyl Peptide Receptor 1 Signaling in Acute Inflammation and Neural Differentiation Induced by Traumatic Brain Injury

Fusco

Gugliandolo

Siracusa

et al. 2020

Biology

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Traumatic brain injury (TBI) is a shocking disease frequently followed by behavioral disabilities, including risk of cerebral atrophy and dementia. N-formylpeptide receptor 1 (FPR1) is expressed in cells and neurons in the central nervous system. It is involved in inflammatory processes and during the differentiation process in the neural stem cells. We investigate the effect of the absence of Fpr1 gene expression in mice subjected to TBI from the early stage of acute inflammation to neurogenesis and systematic behavioral testing four weeks after injury. C57BL/6 animals and Fpr1 KO mice were subjected to TBI and sacrificed 24 h or four weeks after injury. Twenty-four hours after injury, TBI Fpr1 KO mice showed reduced histological impairment, tissue damage and acute inflammation (MAPK activation, NF-κB signaling induction, NRLP3 inflammasome pathway activation and oxidative stress increase). Conversely, four weeks after TBI, the Fpr1 KO mice showed reduced survival of the proliferated cells in the Dentate Gyrus compared to the WT group. Behavioral analysis confirmed this trend. Moreover, TBI Fpr1 KO animals displayed reduced neural differentiation (evaluated by beta-III tubulin expression) and upregulation of astrocyte differentiation (evaluated by GFAP expression). Collectively, our study reports that, immediately after TBI, Fpr1 increased acute inflammation, while after four weeks, Fpr1 promoted neurogenesis.

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Traumatic Brain Injury Stimulates Neural Stem Cell Proliferation via Mammalian Target of Rapamycin Signaling Pathway Activation

Cited by 25 publications

References 83 publications

Zerumbone promotes proliferation of endogenous neural stem cells in vascular dementia by regulating Notch signalling

Zerumbone promotes proliferation of endogenous neural stem cells in vascular dementia by regulating Notch signalling

Traumatic Brain Injury Altered Normal Brain Signaling Pathways: Implications for Novel Therapeutics Approaches

Formyl Peptide Receptor 1 Signaling in Acute Inflammation and Neural Differentiation Induced by Traumatic Brain Injury

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