Bench to Bedside of Neural Stem Cell in Traumatic Brain Injury

Ugoya, SO; Tu, Jian

doi:10.1155/2012/141624

Cited by 17 publications

(12 citation statements)

References 64 publications

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“…3 Initial forces can also disrupt the blood brain barrier, further aggravated by early expression of high concentrations of glucose transporter-1 and synthesis and release of nitric oxide. 4 Consequently, the resulting cerebral haemorrhage and oedema can increase intracranial pressure and lead to cerebral ischaemia. The secondary phase starts a few hours after the injury and can last several days.…”

Section: Pathophysiology Of Traumatic Brain Injurymentioning

confidence: 99%

Cell-Based therapy for traumatic brain injury

Gennai

Monsel

Qin

et al. 2015

British Journal of Anaesthesia

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Traumatic brain injury is a major economic burden to hospitals in terms of emergency department visits, hospitalizations, and utilization of intensive care units. Current guidelines for the management of severe traumatic brain injuries are primarily supportive, with an emphasis on surveillance (i.e. intracranial pressure) and preventive measures to reduce morbidity and mortality. There are no direct effective therapies available. Over the last fifteen years, pre-clinical studies in regenerative medicine utilizing cell-based therapy have generated enthusiasm as a possible treatment option for traumatic brain injury. In these studies, stem cells and progenitor cells were shown to migrate into the injured brain and proliferate, exerting protective effects through possible cell replacement, gene and protein transfer, and release of anti-inflammatory and growth factors. In this work, we reviewed the pathophysiological mechanisms of traumatic brain injury, the biological rationale for using stem cells and progenitor cells, and the results of clinical trials using cell-based therapy for traumatic brain injury. Although the benefits of cell-based therapy have been clearly demonstrated in pre-clinical studies, some questions remain regarding the biological mechanisms of repair and safety, dose, route and timing of cell delivery, which ultimately will determine its optimal clinical use.

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Section: Pathophysiology Of Traumatic Brain Injurymentioning

confidence: 99%

Cell-Based therapy for traumatic brain injury

Gennai

Monsel

Qin

et al. 2015

British Journal of Anaesthesia

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“…Successful in vivo detection and migration monitoring of SPIO-labeled cells was demonstrated in numerous preclinical studies related to implantation of hematopoietic, mesenchymal or neuronal cells in the CNS. 40, 42-44 Clinical trials based on this approach involved tracking autologous neural stem cells by MRI in traumatic head injury and bone marrow stem cells in chronic spinal cord injury and were shown to be safe and effective. 45, 46 Despite the encouraging results of initial trials, cell tracking using SPIO labels is limited by dilution of contrast agent during cellular proliferation, possible transfer of label from dying cells to surrounding endogenous cells (e.g.…”

Section: Biomarker Discovery Bioimaging and Theranosticsmentioning

confidence: 99%

Nanoneuromedicines for degenerative, inflammatory, and infectious nervous system diseases

Gendelman

Anantharam

Bronich

et al. 2015

Nanomedicine: Nanotechnology, Biology and Medicine

106

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Interest in nanoneuromedicine has grown rapidly due to the immediate need for improved biomarkers and therapies for psychiatric, developmental, traumatic, inflammatory, infectious and degenerative nervous system disorders. These, in whole or in part, are a significant societal burden due to growth in numbers of affected people and in disease severity. Lost productivity of the patient and his or her caregiver, and the emotional and financial burden cannot be overstated. The need for improved health care, treatment and diagnostics are immediate. A means to such an end is nanotechnology. Indeed, recent developments of health-care enabling nanotechnologies and nanomedicines range from biomarker discovery including neuroimaging to therapeutic applications for degenerative, inflammatory and infectious disorders of the nervous system. This review focuses on the current and future potential of the field to positively affect clinical outcomes.

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“…Environmental stressors include ischemic sugar/oxygen deprivation, inflammatory cytokine release, the release of excitatory neurotransmitters, and metabolic depression. This leads to the accumulation of reactive oxygen species (ROS) [2], [3], which plays a major role in the pathophysiology of various kinds of brain damage. The accumulated ROS can damage cellular organelles and induce apoptosis of brain cells if untreated.…”

Section: Introductionmentioning

confidence: 99%

Specificity protein 1-zinc finger protein 179 pathway is involved in the attenuation of oxidative stress following brain injury

et al. 2017

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After sudden traumatic brain injuries, secondary injuries may occur during the following days or weeks, which leads to the accumulation of reactive oxygen species (ROS). Since ROS exacerbate brain damage, it is important to protect neurons against their activity. Zinc finger protein 179 (Znf179) was shown to act as a neuroprotective factor, but the regulation of gene expression under oxidative stress remains unknown. In this study, we demonstrated an increase in Znf179 protein levels in both in vitro model of hydrogen peroxide (H2O2)-induced ROS accumulation and animal models of traumatic brain injury. Additionally, we examined the sub-cellular localization of Znf179, and demonstrated that oxidative stress increases Znf179 nuclear shuttling and its interaction with specificity protein 1 (Sp1). Subsequently, the positive autoregulation of Znf179 expression, which is Sp1-dependent, was further demonstrated using luciferase reporter assay and green fluorescent protein (GFP)-Znf179-expressing cells and transgenic mice. The upregulation of Sp1 transcriptional activity induced by the treatment with nerve growth factor (NGF) led to an increase in Znf179 levels, which further protected cells against H2O2-induced damage. However, Sp1 inhibitor, mithramycin A, was shown to inhibit NGF effects, leading to a decrease in Znf179 expression and lower cellular protection. In conclusion, the results obtained in this study show that Znf179 autoregulation through Sp1-dependent mechanism plays an important role in neuroprotection, and NGF-induced Sp1 signaling may help attenuate more extensive (ROS-induced) damage following brain injury.

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Bench to Bedside of Neural Stem Cell in Traumatic Brain Injury

Cited by 17 publications

References 64 publications

Cell-Based therapy for traumatic brain injury

Cell-Based therapy for traumatic brain injury

Nanoneuromedicines for degenerative, inflammatory, and infectious nervous system diseases

Specificity protein 1-zinc finger protein 179 pathway is involved in the attenuation of oxidative stress following brain injury

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