Faculty Opinions recommendation of Spiking and nonspiking classes of oligodendrocyte precursor glia in CNS white matter.

2008 ◽  
Author(s):  
Michael Fehlings
Keyword(s):  
White Matter ◽  
Oligodendrocyte Precursor

Ginkgolide B promotes oligodendrocyte precursor cell differentiation and survival via Akt/CREB/bcl-2 signaling pathway after white matter lesion

2021 ◽  
pp. 153537022198995
Author(s):  
Jian Huang ◽  
Jun Yang ◽  
Xingju Zou ◽  
Shilun Zuo ◽  
Jing Wang ◽  
...  
Keyword(s):  
White Matter ◽  
White Matter Lesion ◽  
Neuroprotective Effect ◽  
Precursor Cell ◽  
Cerebral Hypoperfusion ◽  
Ginkgolide B ◽  
Oligodendrocyte Precursor Cell ◽  
Learning Abilities ◽  
Phosphorylated Akt ◽  
Oligodendrocyte Precursor

White matter lesion (WML) is caused by chronic cerebral hypoperfusion, which are usually associated with cognitive impairment. Evidence from recent studies has shown that ginkgolide B has a neuroprotective effect that could be beneficial for the treatment of ischemia; however, it is not clear whether ginkgolide B has a protective effect on WML. Our data show that ginkgolide B can promote the differentiation of oligodendrocyte precursor cell (OPC) into oligodendrocytes and promote oligodendrocyte survival following a WML. Ginkgolide B (5, 10, 20 mg/kg) or saline is administered intraperitoneally every day after WML. After 4 weeks, the data of Morris water maze suggested that rats’ memory and learning abilities were impaired, and the administration of ginkgolide B enhanced behavioral achievement. Also, treatment with ginkgolide B significantly attenuated this loss of myelin. Our result suggests that ginkgolide B promotes the differentiation of OPC into oligodendrocytes. We also found that ginkgolide B ameliorates oligodendrocytes apoptosis. Furthermore, ginkgolide B enhanced the expression of phosphorylated Akt and CREB. In conclusion, our data firstly show that ginkgolide B promotes oligodendrocyte genesis and oligodendrocyte myelin following a WML, possibly involving the Akt and CREB pathways.

scholarly journals Spiking and nonspiking classes of oligodendrocyte precursor glia in CNS white matter

2008 ◽  
Vol 11 (4) ◽  
pp. 450-456 ◽  
Author(s):  
Ragnhildur Káradóttir ◽  
Nicola B Hamilton ◽  
Yamina Bakiri ◽  
David Attwell
Keyword(s):  
White Matter ◽  
Oligodendrocyte Precursor

scholarly journals Vanishing White Matter Disease Expression of Truncated EIF2B5 Activates Induced Stress Response

2020 ◽  
Author(s):  
Matthew D. Keefe ◽  
Haille E. Soderholm ◽  
Hung-Yu Shih ◽  
Tamara J. Stevenson ◽  
Kathryn A. Glaittli ◽  
...  
Keyword(s):  
White Matter ◽  
Motor Behavior ◽  
Somatic Growth ◽  
Initiation Factor ◽  
White Matter Disease ◽  
The Central Nervous System ◽  
Oligodendrocyte Precursor ◽  
Vanishing White Matter Disease ◽  
Development And Validation ◽  
Vanishing White Matter

AbstractVanishing White Matter disease (VWM) is a severe leukodystrophy of the central nervous system caused by mutations in subunits of the eukaryotic initiation factor 2B complex (eIF2B). Current models only partially recapitulate key disease features, and pathophysiology is poorly understood. Through development and validation of zebrafish (Danio rerio) models of VWM, we demonstrate that zebrafish eif2b mutants phenocopy VWM, including impaired somatic growth, early lethality, impaired myelination, loss of oligodendrocyte precursor cells, increased apoptosis in the CNS, and impaired motor swimming behavior. Expression of human EIF2B2 in the zebrafish eif2b2 mutant rescues lethality and CNS apoptosis, demonstrating conservation of function between zebrafish and human. In the mutants, intron 12 retention leads to expression of a truncated eif2b5 transcript. Expression of the truncated eif2b5 in wild-type larva impairs motor behavior and activates the ISR, suggesting that a feed-forward mechanism in VWM is a significant component of disease pathophysiology.

Abstract TMP30: M2 Microglia Derived Exosomes Promote White Matter Repair and Long-Term Functional Recovery After Focal Cerebral Ischemia in Mice

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Yongfang Li ◽  
Longlong Luo ◽  
Zhijun Zhang ◽  
Yaohui Tang ◽  
Guo-Yuan Yang
Keyword(s):  
White Matter ◽  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Oligodendrocyte Precursor Cells ◽  
Oligodendrocyte Precursor Cell ◽  
M2 Microglia ◽  
Oligodendrocyte Precursor ◽  
White Matter Repair ◽  
Exosomal Mirna

Objectives: White matter injury aggravates neurological and cognitive impairment in experimental ischemic stroke. M2 microglia promote oligodendrocyte precursor cells survival and differentiation, and further enhance white matter repair. However, the molecular mechanism is unclear. Here, we explored the effect and mechanism of M2 microglia-derived exosomes on white matter repair after focal cerebral ischemia in mice. Methods: Microglia BV2 cells were polarized to M2 phenotype by IL-4 stimulation. Exosomes were isolated from M2 microglia (M2-Exo) and unstimulated microglia as a control (M0-Exo). M2-Exo and M0-Exo (100 μg) were intravenously injected after 90-minute middle cerebral artery occlusion in mice (n=72). Brain atrophy volume and neuro behavioral outcomes were examined in 28 days following focal cerebral ischemia. Oligodendrocyte precursor cells survival, differentiation and white matter integrity were evaluated. Exosomal miRNA and target gene were further examined to explore molecular mechanism. Results: M2-Exo treatment promoted sensorimotor and memory function recovery ( p <0.05), and further reduced brain atrophy compared to the M0-Exo control group ( p <0.001). Immunostaining showed that M2-Exo increased the number of BrdU + /Pdgfr-α + and BrdU + /adenomatous polyposis coli + cells, enhanced myelin basic protein fluorescence-intensity compared to the control ( p <0.05). M2-Exo increased oligodendrocyte precursor cell survival under OGD in vi tro , ( p <0.05) and differentiation ( p <0.05). Exosomal miRNA sequencing and PCR identified that miR-23a-5p was enriched in M2-Exo. Conclusion: Our results showed that M2-Exo treatment enhanced oligodendrocyte precursor cell survival and differentiation, further promoted white matter repair and long-term functional recovery, suggesting that M2-Exo is a novel therapeutic strategy for the white matter repair after ischemic brain injury.

scholarly journals White Matter and Neuroprotection in Alzheimer’s Dementia

Molecules ◽  
2020 ◽  
Vol 25 (3) ◽  
pp. 503 ◽  
Author(s):  
Luca Lorenzini ◽  
Mercedes Fernandez ◽  
Vito Antonio Baldassarro ◽  
Andrea Bighinati ◽  
Alessandro Giuliani ◽  
...  
Keyword(s):  
White Matter ◽  
Alzheimer’S Dementia ◽  
Oligodendrocyte Precursor Cells ◽  
Resonance Imaging ◽  
Alzheimer's Dementia ◽  
The Central Nervous System ◽  
Oligodendrocyte Precursor ◽  
Main Component ◽  
Preclinical And Clinical Studies

Myelin is the main component of the white matter of the central nervous system (CNS), allowing the proper electrical function of the neurons by ensheathing and insulating the axons. The extensive use of magnetic resonance imaging has highlighted the white matter alterations in Alzheimer’s dementia (AD) and other neurodegenerative diseases, alterations which are early, extended, and regionally selective. Given that the white matter turnover is considerable in the adulthood, and that myelin repair is currently recognized as being the only true reparative capability of the mature CNS, oligodendrocyte precursor cells (OPCs), the cells that differentiate in oligodendrocyte, responsible for myelin formation and repair, are regarded as a potential target for neuroprotection. In this review, several aspects of the OPC biology are reviewed. The histology and functional role of OPCs in the neurovascular-neuroglial unit as described in preclinical and clinical studies on AD is discussed, such as the OPC vulnerability to hypoxia-ischemia, neuroinflammation, and amyloid deposition. Finally, the position of OPCs in drug discovery strategies for dementia is discussed.

scholarly journals Vanishing white matter disease expression of truncated EIF2B5 activates induced stress response

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Matthew D Keefe ◽  
Haille E Soderholm ◽  
Hung-Yu Shih ◽  
Tamara J Stevenson ◽  
Kathryn A Glaittli ◽  
...  
Keyword(s):  
White Matter ◽  
Motor Behavior ◽  
Somatic Growth ◽  
Initiation Factor ◽  
White Matter Disease ◽  
The Central Nervous System ◽  
Oligodendrocyte Precursor ◽  
Vanishing White Matter Disease ◽  
Development And Validation ◽  
Vanishing White Matter

Vanishing white matter disease (VWM) is a severe leukodystrophy of the central nervous system caused by mutations in subunits of the eukaryotic initiation factor 2B complex (eIF2B). Current models only partially recapitulate key disease features, and pathophysiology is poorly understood. Through development and validation of zebrafish (Danio rerio) models of VWM, we demonstrate that zebrafish eif2b mutants phenocopy VWM, including impaired somatic growth, early lethality, effects on myelination, loss of oligodendrocyte precursor cells, increased apoptosis in the CNS, and impaired motor swimming behavior. Expression of human EIF2B2 in the zebrafish eif2b2 mutant rescues lethality and CNS apoptosis, demonstrating conservation of function between zebrafish and human. In the mutants, intron 12 retention leads to expression of a truncated eif2b5 transcript. Expression of the truncated eif2b5 in wild-type larva impairs motor behavior and activates the ISR, suggesting that a feed-forward mechanism in VWM is a significant component of disease pathophysiology.

Oligodendrocyte precursor cell transplantation promotes angiogenesis and remyelination via Wnt/β-catenin pathway in a mouse model of middle cerebral artery occlusion

2021 ◽  
pp. 0271678X2110653
Author(s):  
Li-Ping Wang ◽  
Jiaji Pan ◽  
Yongfang Li ◽  
Jieli Geng ◽  
Chang Liu ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
White Matter ◽  
Cell Transplantation ◽  
Artery Occlusion ◽  
Precursor Cells ◽  
Precursor Cell ◽  
Oligodendrocyte Precursor Cells ◽  
Oligodendrocyte Precursor Cell ◽  
Oligodendrocyte Precursor ◽  
Cerebral Artery Occlusion

White matter injury is a critical pathological characteristic during ischemic stroke. Oligodendrocyte precursor cells participate in white matter repairing and remodeling during ischemic brain injury. Since oligodendrocyte precursor cells could promote Wnt-dependent angiogenesis and migrate along vasculature for the myelination during the development in the central nervous system, we explore whether exogenous oligodendrocyte precursor cell transplantation promotes angiogenesis and remyelination after middle cerebral artery occlusion in mice. Here, oligodendrocyte precursor cell transplantation improved motor and cognitive function, and alleviated brain atrophy. Furthermore, oligodendrocyte precursor cell transplantation promoted functional angiogenesis, and increased myelin basic protein expression after ischemic stroke. The further study suggested that white matter repairing after oligodendrocyte precursor cell transplantation depended on angiogenesis induced by Wnt/β-catenin signal pathway. Our results demonstrated a novel pathway that Wnt7a from oligodendrocyte precursor cells acting on endothelial β-catenin promoted angiogenesis and improved neurobehavioral outcomes, which facilitated white matter repair and remodeling during ischemic stroke.

scholarly journals Inhibition of Mitochondrial ROS by MitoQ Alleviates White Matter Injury and Improves Outcomes after Intracerebral Haemorrhage in Mice

2020 ◽  
Vol 2020 ◽  
pp. 1-12 ◽  
Author(s):  
Weixiang Chen ◽  
Chao Guo ◽  
Zhengcai Jia ◽  
Jie Wang ◽  
Min Xia ◽  
...  
Keyword(s):  
White Matter ◽  
Intracerebral Haemorrhage ◽  
Motor Evoked Potential ◽  
White Matter Injury ◽  
Antioxidant Treatment ◽  
Evidence Based Treatment ◽  
Mitochondrial Ros ◽  
Ros Scavenger ◽  
Oligodendrocyte Precursor

White matter injury (WMI) is an important cause of high disability after intracerebral haemorrhage (ICH). It is widely accepted that reactive oxygen species (ROS) contributes to WMI, but there is still no evidence-based treatment. Here, mitoquinone (MitoQ), a newly developed selective mitochondrial ROS scavenger, was used to test its neuroprotective potential. The data showed that MitoQ attenuated motor function deficits and motor-evoked potential (MEP) latency prolongation. Further research found that MitoQ blunted the loss of oligodendrocytes and oligodendrocyte precursor cells, therefore reduced demyelination and axon swelling after ICH. In the in vitro experiments, MitoQ, but not the nonselective antioxidant, almost completely attenuated the iron-induced membrane potential decrease and cell death. Mechanistically, MitoQ blocked the ATP deletion and mitochondrial ROS overproduction. The present study demonstrates that the selective mitochondrial ROS scavenger MitoQ may improve the efficacy of antioxidant treatment of ICH by white matter injury alleviation.

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