Neuroprotective effects of neuroglobin after mechanical injury

Shang, Aijia; Kai-Dong, Liu; Wang, Hangyan; Wang, Jing; Hang, Xingyi; Yang, Ying; Wang, Zhongfeng; Zhang, Chenggang; Zhou, Ding-biao

doi:10.1007/s10072-011-0772-4

Cited by 16 publications

(13 citation statements)

References 19 publications

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“…A recent study showed that over-expression of Ngb in cultured neurons was neuroprotective against mechanical injury in vitro. This study also showed increased Ngb expression levels with peak time of 6 hours after TBI, and these increased levels correlated to the severity of TBI in rats [23]. Thus, we picked only the time point of 6 hours after TBI for examining changes of Ngb expression and 3NT production after TBI in present study.…”

Section: Resultsmentioning

confidence: 94%

“…This examination by immunohistochemistry (Figure 1A) and western blot analysis (Figure 1B) was consistent with a report that showed a transient increase of brain Ngb expression with peak at 6 h after TBI in rats. That study also showed Ngb over-expression decreased mechanical injury-induced neuron death [23]. In our present study, quantification of western blot analysis showed that the basal levels of Ngb protein expression (149% of WT sham control mice) and the CCI-induced increase of Ngb protein levels at 6 h after TBI (196% of WT sham control mice) were significantly higher in Ngb-Tg mouse brains compared to WT TBI controls (147% of WT sham control mice) (Figure1C).…”

Section: Resultsmentioning

confidence: 99%

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Neuroglobin-overexpression reduces traumatic brain lesion size in mice

Zhao

et al. 2012

BMC Neurosci

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BackgroundAccumulating evidence has demonstrated that over-expression of Neuroglobin (Ngb) is neuroprotective against hypoxic/ischemic brain injuries. In this study we tested the neuroprotective effects of Ngb over-expression against traumatic brain injury (TBI) in mice.ResultsBoth Ngb over-expression transgenic (Ngb-Tg) and wild-type (WT) control mice were subjected to TBI induced by a controlled cortical impact (CCI) device. TBI significantly increased Ngb expression in the brains of both WT and Ngb-Tg mice, but Ngb-Tg mice had significantly higher Ngb protein levels at the pre-injury baseline and post-TBI. Production of oxidative tissue damage biomarker 3NT in the brain was significantly reduced in Ngb-Tg mice compared to WT controls at 6 hours after TBI. The traumatic brain lesion volume was significantly reduced in Ngb Tg mice compared to WT mice at 3 weeks after TBI; however, there were no significant differences in the recovery of sensorimotor and spatial memory functional deficits between Ngb-Tg and WT control mice for up to 3 weeks after TBI.ConclusionNgb over-expression reduced traumatic lesion volume, which might partially be achieved by decreasing oxidative stress.

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Section: Resultsmentioning

confidence: 94%

Section: Resultsmentioning

confidence: 99%

Neuroglobin-overexpression reduces traumatic brain lesion size in mice

Zhao

et al. 2012

BMC Neurosci

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“…In addition to its ability to bind oxygen, neuroglobin also functions as an antioxidant and free radical scavenger [18]. Neuroglobin is expressed throughout the central and peripheral nervous systems of vertebrates [4, 14, 23, 28]. The primary sites of neuroglobin expression are the limbic system and cerebral cortex [14].…”

Section: Introductionmentioning

confidence: 99%

Neuroglobin overexpression improves sensorimotor outcomes in a mouse model of traumatic brain injury

Taylor

Kelley

Gregory

et al. 2014

Neuroscience Letters

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There is a significant need for novel treatments that will improve traumatic brain injury (TBI) outcomes. One potential neuroprotective mechanism is to increase oxygen binding proteins such as neuroglobin. Neuroglobin has a high affinity for oxygen, is an effective free radical scavenger, and is neuroprotective within the brain following hypoxia and ischemia. The purpose of this study was to determine whether neuroglobin overexpression improves sensorimotor outcomes following TBI in transgenic neuroglobin overexpressing (NGB) mice. Additional study aims were to determine if and when an endogenous neuroglobin response occurred following TBI in wild-type (WT) mice, and in what brain regions and cell types the response occurred. Controlled cortical impact (CCI) was performed in adult (5 month) C57/BL6 WT mice, and NGB mice constitutively overexpressing neuroglobin via the chicken beta actin promoter coupled with the cytomegalovirus distal enhancer. The gridwalk task was used for sensorimotor testing of both WT and NGB mice, prior to injury, and at 2, 3, and 7 days post-TBI. NGB mice displayed significant reductions in the average number of foot faults per minute walking at 2, 3, and 7 days post-TBI when compared to WT mice at each time point. Neuroglobin mRNA expression was assessed in the injured cortex of WT mice prior to injury, and at 1, 3, 7, and 14 days post-TBI using quantitative real time polymerase chain reaction (qRT-PCR). Neuroglobin mRNA was significantly increased at 7 days post-TBI. Immunostaining showed neuroglobin primarily localized to neurons and glial cells in the injured cortex and ipsilateral hippocampus of WT mice, while neuroglobin was present in all brain regions of NGB mice at 7 days post-TBI. These results showed that overexpression of neuroglobin reduced sensorimotor deficits following TBI, and that an endogenous increase in neuroglobin expression occurs during the subacute period. Increasing neuroglobin expression through novel therapeutic interventions during the acute period after TBI may improve recovery.

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“…Multiple neuroprotective effects operate by different mechanisms, including inhibit calcium in ux, reduce cellular uptake of iron, copper, and zinc, suppress necrosis and apoptosis, and several studies suggest that NGB may positively affect TBI outcomes [32,33]. The reported results indicated that there was a late, but signi cant, increase in NGB mRNA expression 7 days post-TBI in WT mice and the subacute increase occurred later that were known to be upregulated at 3 days post-TBI [32].The previous work in the rat and mouse also showed increased NGB expression levels with peak time of 6 hours after TBI [34].…”

Section: Introductionmentioning

confidence: 67%

Amyloid-β Protein and Neuroglobin Protein as Biomarkers on Brainstem Following Traumatic Brain Injury in Rats

Zhu

Liang³

et al. 2020

Preprint

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Abstract Background: Biomarkers play an important role in accurate diagnosis of traumatic brain injury (TBI). Due to the complexity and diversity of TBI, it is likely that a single biomarker will not be used for exactly diagnose. Amyloid-beta (Aβ) protein is generated by sequential cleavage of amyloid precursor protein (APP) by β- and γ-secretase, which may exert its toxic effects by increasing reactive oxygen species and neuroinflammation in the brain as damage factor of TBI. Its use in diagnosis for TBI is becoming more widespread. Neuroglobin (NGB) protein is great potential to diminish neuronal damage. Most epidemiological evidence suggested that Aβ and NGB may be used as biomarkers on brainstem (BS) following TBI. The aim of this study was to investigate the trend of Aβ and NGB on BS of rats with TBI and to analyze comprehensively them as potential biomarkers. Methods: Adult male Sprague-Dawley rats were subjected to the modified weight-drop model of closed TBI. Biologic behavior observation, histopathological assessments and western blot assay were performed. Aβ and NGB expression indicated temporal changes in BS after TBI. Their accuracy and efficiency of performing these tasks were calculated and statistical comparisons performed.Results: The results of Aβ enable us to speculate that the time points of 3 h, 6 h and 12 h may be crucial points for the diagnosis of TBI. NGB expression in the injured had obvious difference versus the control, the points of 1 h and 3 h were apparently higher than the control, and the groups of 12 h and 48 h were two peaks in the present study. Furthermore, the immunofluorescence assay results supported that Aβ and NGB co-localization in the neuros of BS, and the NGB specific expression in the BS of neurons.Conclusions: Therefore, the expression and change rules of Aβ and NBG in the BS may provide an important foundation for the diagnosis of TBI, damage assessment and therapeutic intervention.

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Neuroprotective effects of neuroglobin after mechanical injury

Cited by 16 publications

References 19 publications

Neuroglobin-overexpression reduces traumatic brain lesion size in mice

Neuroglobin-overexpression reduces traumatic brain lesion size in mice

Neuroglobin overexpression improves sensorimotor outcomes in a mouse model of traumatic brain injury

Amyloid-β Protein and Neuroglobin Protein as Biomarkers on Brainstem Following Traumatic Brain Injury in Rats

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