Stem Cell Therapies for Traumatic Brain Injury

Koliatsos, Vassilis E.; Xu, Leyan; Cummings, Brian J.

doi:10.2217/rme.15.62

Cited by 8 publications

(8 citation statements)

References 20 publications

(7 reference statements)

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“…They are self-renewing, multipotent and undifferentiated precursor cells that have the ability to differentiate into glial and neuronal lineages. NSCs may be useful in cell-based replacement therapies for neurological disorders, including Alzheimer's disease, traumatic brain injury, spinal cord injuries and retinal disease (3)(4)(5). However, poor proliferation and insufficient differentiation of the transplanted NSCs into neurons limit the practical use of NSC-based therapies (6,7), making further study necessary to realize the potential of NSCs in clinical treatment (8)(9)(10).…”

Section: Introductionmentioning

confidence: 99%

Overexpression of miR‑21 promotes neural stem cell proliferation and neural differentiation via the Wnt/β‑catenin signaling pathway in vitro

Zhang

Yang

et al. 2017

Mol Med Report

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The primary aim of the present study was to examine the effects of microRNA‑21 (miR‑21) on the proliferation and differentiation of rat primary neural stem cells (NSCs) in vitro. miR‑21 was overexpressed in NSCs by transfection with a miR‑21 mimic. The effects of miR‑21 overexpression on NSC proliferation were revealed by Cell Counting kit 8 and 5‑ethynyl‑2'‑deoxyuridine incorporation assay, and miR‑21 overexpression was revealed to increase NSC proliferation. miR‑21 overexpression was confirmed using reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR). mRNA and protein expression levels of key molecules (β‑catenin, cyclin D1, p21 and miR‑21) in the Wnt/β‑catenin signaling pathway were studied by RT‑qPCR and western blot analysis. RT‑qPCR and western blot analyses revealed that miR‑21 overexpression increased β‑catenin and cyclin D1 expression, and decreased p21 expression. These results suggested that miR‑21‑induced increase in proliferation was mediated by activation of the Wnt/β‑catenin signaling pathway, since overexpression of miR‑21 increased β‑catenin and cyclin D1 expression and reduced p21 expression. Furthermore, inhibition of the Wnt/β‑catenin pathway with FH535 attenuated the influence of miR‑21 overexpression on NSC proliferation, indicating that the factors activated by miR‑21 overexpression were inhibited by FH535 treatment. Furthermore, overexpression of miR‑21 enhanced the differentiation of NSCs into neurons and inhibited their differentiation into astrocytes. The present study indicated that in primary rat NSCs, overexpression of miR‑21 may promote proliferation and differentiation into neurons via the Wnt/β‑catenin signaling pathway in vitro.

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Section: Introductionmentioning

confidence: 99%

Overexpression of miR‑21 promotes neural stem cell proliferation and neural differentiation via the Wnt/β‑catenin signaling pathway in vitro

Zhang

Yang

et al. 2017

Mol Med Report

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“…. Modulating immune responses through spleen, such as reducing IL-1β, TNF-α, and IL-6 contents, improves outcomes of neural injury(Acosta et al, 2015;Tajiri et al, 2014;Koliatsos et al, 2015;Li et al, 2011). Torso shielding can certainly protect the spleen from blast injury and this effect may attenuate microglial activation reported here.…”

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confidence: 62%

Neuroinflammation in primary blast neurotrauma: Time course and prevention by torso shielding

Schaefer

Linville

et al. 2016

Experimental Neurology

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Mechanisms of primary blast injury caused by overpressure are not fully understood. In particular, the presence and time course of neuroinflammation are unknown and so are the signatures of reactive inflammatory cells, especially the neuroprotective versus injurious roles of microglia. In general, chronic microglial activation in the injured brain suggests a pro-degenerative role for these reactive cells. In this study, we investigated the temporal dynamics of microglial activation in the brain of mice exposed to mild-moderate blast in a shock tube. Because, in our previous work, we had found that torso shielding with rigid Plexiglas attenuates traumatic axonal injury in the brain, we also evaluated neuroinflammatory microglial responses in animals with torso protection at 7 days post blast injury. Because of the prominent involvement of the visual system in blast TBI in rodents, activated microglial cells were counted in the optic tract at various time points post-injury with stereological methods. Cell counts (activated microglial cell densities) from subjects exposed to blast TBI were compared with counts from corresponding sham animals. We found that mild-moderate blast injury causes focal activation of microglia in certain white matter tracts, including the visual pathway. In the optic tract, the density of activated microglial profiles gradually intensified from 3 to 15 days post-injury and then became attenuated at 30 days. Torso protection significantly reduced microglial activation at 7 days. These findings shed light into mechanisms of primary blast neurotrauma and may suggest novel diagnostic and monitoring methods for patients. They leave open the question of whether microglial activation post blast is protective or detrimental, although response is time limited. Finally, our findings confirm the protective role of torso shielding and stress the importance of improved or optimized body gear for warfighters or other individuals at risk for blast exposure.

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“…Regenerative medicine as an important part of modern medicine aims at replacing or regenerating cells, tissues, or organs to restore or establish normal function. 36 Stem cells have the ability of selfrenewing and differentiating into various cell lineages, and stem cellbased strategies hold promise in curing traumatic brain injury [37][38][39] and stroke. [40][41][42] Our group has done much work in identifying therapeutic targets and screening effective neuroprotective drugs against stroke.…”

Section: Regenerative Medicinementioning

confidence: 99%

Organoid technology for brain and therapeutics research

Wang

et al. 2017

CNS Neurosci Ther

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Brain is one of the most complex organs in human. The current brain research is mainly based on the animal models and traditional cell culture. However, the inherent species differences between humans and animals as well as the gap between organ level and cell level make it difficult to study human brain development and associated disorders through traditional technologies. Recently, the brain organoids derived from pluripotent stem cells have been reported to recapitulate many key features of human brain in vivo, for example recapitulating the zone of putative outer radial glia cells. Brain organoids offer a new platform for scientists to study brain development, neurological diseases, drug discovery and personalized medicine, regenerative medicine, and so on. Here, we discuss the progress, applications, advantages, limitations, and prospects of brain organoid technology in neurosciences and related therapeutics.

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Stem Cell Therapies for Traumatic Brain Injury

Cited by 8 publications

References 20 publications

Overexpression of miR‑21 promotes neural stem cell proliferation and neural differentiation via the Wnt/β‑catenin signaling pathway in vitro

Overexpression of miR‑21 promotes neural stem cell proliferation and neural differentiation via the Wnt/β‑catenin signaling pathway in vitro

Neuroinflammation in primary blast neurotrauma: Time course and prevention by torso shielding

Organoid technology for brain and therapeutics research

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