Cellular and temporal expression of NADPH oxidase (NOX) isotypes after brain injury

Cooney, Sean J.; Bermudez-Sabogal, Sara L; Byrnes, Kimberly R.

doi:10.1186/1742-2094-10-155

Cited by 112 publications

(133 citation statements)

References 56 publications

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“…NOX4 expression in neurons peaked at 24-48 h after injury, and the positive rate of NOX4 expression in astrocytes increased gradually as the duration of injury increased. The fact that NOX2 expression in neurons peaks at 24 h after injury in clinical patients is consistent with finding in animal experiments [17]. The results of our study, combined with the results of animal studies suggest that after TBI high expressions of NOX2 and NOX4 lead to high levels of ROS production, resulting in OS reaction, which triggers repeated or multiple brain injuries [17].…”

Section: Discussionsupporting

confidence: 93%

“…The fact that NOX2 expression in neurons peaks at 24 h after injury in clinical patients is consistent with finding in animal experiments [17]. The results of our study, combined with the results of animal studies suggest that after TBI high expressions of NOX2 and NOX4 lead to high levels of ROS production, resulting in OS reaction, which triggers repeated or multiple brain injuries [17]. The purpose of our clinical study was to explore the temporal correlation of NOX2 and NOX4 expression in neurons and astrocytes of TBI patients, to provide a theoretical basis for future treatment of repeated or multiple injuries caused by TBI.…”

Section: Discussionsupporting

confidence: 88%

“…Studies on NOX4 have been focusing on its role in vascular endothelium regeneration, and it is believed that NOX4 is a key factor in promoting the regeneration of endothelium. Therefore, NOX4 may also play an important role in brain injury repair [17][18][19].…”

Section: Introductionmentioning

confidence: 99%

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Expression and clinical significance of non-phagocytic cell oxidase 2 and 4 after human traumatic brain injury

Tian

Zhong

et al. 2014

Neurol Sci

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The goal of this study was to examine NOX2 and NOX4 expression in clinical samples of patients with traumatic brain injury (TBI), and to explore the correlation of NOX2 and NOX4 expression with the severity of injury, duration of injury, and prognosis. Brain samples of 20 TBI patients within 1 cm of the contusion site were collected and grouped based on duration of injury, Glasgow Coma Scale (GCS) and Glasgow Outcome Scale (GOS), and immunofluorescence staining were performed to examine the expression levels of NOX2 and NOX4 in the neurons and astrocytes. We found that the expression level of NOX2 in neurons and positive rate of NOX2 expression in astrocytes peaked at 12-24 and 6-12 h after injury, respectively. The expression level of NOX4 in neurons peaked at 24-48 h, and the positive rate of NOX4 expression gradually increased with prolonged injury. We also found that the higher the GCS score, the lower the expression levels of NOX2 and NOX4 in neurons was, while higher the GCS score, the lower the positive rate of NOX4 expression in astrocytes was and the higher the GOS grade, the lower the positive rate of expression in astrocytes was. In conclusion, NOX2 and NOX4 expressions significantly increase at an early stage after TBI, and abnormal expressions of NOX2 and NOX4 are correlated to patient prognosis to certain extent.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 88%

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Expression and clinical significance of non-phagocytic cell oxidase 2 and 4 after human traumatic brain injury

Tian

Zhong

et al. 2014

Neurol Sci

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“…Cellular expression of NOX in the central nervous system (CNS) appears to be isotype dependent[6]. In particular, the NOX2, 3 and 4 isotypes have been identified in CNS cells, particularly after stimulation or activation.…”

Section: Introductionmentioning

confidence: 99%

Characterization of the expression and inflammatory activity of NADPH oxidase after spinal cord injury

Cooney

Zhao

Byrnes

2014

Free Radical Research

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Reactive oxygen species and the NADPH oxidase (NOX) enzyme are both up-regulated after spinal cord injury (SCI) and play significant roles in promoting post-injury inflammation. However, the cellular and temporal expression profile of NOX isotypes, including NOX2, 3 and 4, after SCI is currently unclear. The purpose of this study was to resolve this expression profile and examine the effect of inhibition of NOX on inflammation after SCI. Briefly, adult male rats were subjected to moderate contusion SCI. Double immunofluorescence for NOX isotypes and CNS cellular types was performed at 24 hours, 7 days and 28 days post-injury. NOX isotypes were found to be expressed in neurons, astrocytes and microglia, and this expression was dependent on injury status. NOX2 and 4 were found in all cell types assessed, while NOX3 was positively identified in neurons only. NOX2 was the most responsive to injury, increasing in both microglia and astrocytes. The biggest increases in expression were observed at 7 days post-injury and increased expression was maintained through 28 days. NOX2 inhibition by systemic administration of gp91ds-tat at 15 minutes, 6 hours or 7 days after injury reduced both pro-inflammatory cytokine expression and evidence of oxidative stress in the injured spinal cord. This study therefore illustrates the regional and temporal influence on NOX isotype expression and the importance of NOX activation in SCI. This information will be useful in future studies of understanding reactive oxygen species production after injury and therapeutic potentials.

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“…39 In the case of TBI, mitochondria are considered the major source of ROS production, 40 but NADPH oxidase is also likely to play the role. 41 In this study, we observed that NADPH oxidase was a source of ROS production in response to the concussion. NADPH oxidase activity can peak early at 1 h after TBI, followed by a secondary peak that appears between 24 and 96 h postinjury.…”

Section: Discussionmentioning

confidence: 72%

Suppression of Oxidative Stress and 5-Lipoxygenase Activation by Edaravone Improves Depressive-Like Behavior after Concussion

Higashi

Hoshijima²,

Yawata³

et al. 2014

Journal of Neurotrauma

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Brain concussions are a serious public concern and are associated with neuropsychiatric disorders, such as depression. Patients with concussion who suffer from depression often experience distress. Nevertheless, few pre-clinical studies have examined concussion-induced depression, and there is little information regarding its pharmacological management. Edaravone, a free radical scavenger, can exert neuroprotective effects in several animal models of neurological disorders. However, the effectiveness of edaravone in animal models of concussion-induced depression remains unclear. In this study, we examined whether edaravone could prevent concussion-induced depression. Mice were subjected to a weightdrop injury and intravenously administered edaravone (3.0 mg/kg) or vehicle immediately after impact. Serial magnetic resonance imaging showed no abnormalities of the cerebrum on diffusion T1-and T2-weighted images. We found that edaravone suppressed concussion-induced depressive-like behavior in the forced swim test, which was accompanied by inhibition of increased hippocampal and cortical oxidative stress (OS) and suppression of 5-lipoxygenase (5-LOX) translocation to the nuclear envelope in hippocampal astrocytes. Hippocampal OS in concussed mice was also prevented by the nicotinamide adenine dinucleotide phosphate oxidase inhibitor, apocynin, and administration of BWB70C, a 5-LOX inhibitor, immediately and 24 h after injury prevented depressive-like behaviors in concussed mice. Further, antidepressant effects of edaravone were observed in mice receiving 1.0 or 3.0 mg/kg of edaravone immediately after impact, but not at a lower dose of 0.1 mg/kg. This antidepressant effect persisted up to 1 h after impact, whereas edaravone treatment at 3 h after impact had no effect on concussion-induced depressive-like behavior. These results suggest that edaravone protects against concussion-induced depression, and this protection is mediated by suppression of OS and 5-LOX translocation.

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Cellular and temporal expression of NADPH oxidase (NOX) isotypes after brain injury

Cited by 112 publications

References 56 publications

Expression and clinical significance of non-phagocytic cell oxidase 2 and 4 after human traumatic brain injury

Expression and clinical significance of non-phagocytic cell oxidase 2 and 4 after human traumatic brain injury

Characterization of the expression and inflammatory activity of NADPH oxidase after spinal cord injury

Suppression of Oxidative Stress and 5-Lipoxygenase Activation by Edaravone Improves Depressive-Like Behavior after Concussion

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