Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Distribution of the Immunoreactivity for Glycoprotein M6B in the Neurogenic Niche and Reactive Glia in the Injury Penumbra Following Traumatic Brain Injury in Mice.

ABSTRACT: The location and morphology of astrocytes are known to contribute to their diversity, and this diversity is often associated with their selective functions. However, molecular markers for astrocyte subtypes are largely unknown. In this study, we found that the immunoreactivity for glycoprotein GPM6B (M6B-IR) is preferentially expressed in the astrocytes associated with ventricles or neurogenic regions of the adult mouse brain. In particular, M6B-IR in the neurogenic niche was confined to glial fibrillary acidic protein- or nestin-expressing neural stem cells. Furthermore, in the injury penumbra, reactive astrocytes expressing nestin also exhibited strong M6B-IR. These results reveal that GPM6B is a potential molecular marker for a subset of astrocytes, as well as for the injury-dependent activation of astrocytes.

SUBMITTER: Choi KM

PROVIDER: S-EPMC3897689 | biostudies-literature | 2013 Dec

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Publications

Distribution of the Immunoreactivity for Glycoprotein M6B in the Neurogenic Niche and Reactive Glia in the Injury Penumbra Following Traumatic Brain Injury in Mice.

Choi Kyung Mee KM Kim Joo Yeon JY Kim Younghwa Y

Experimental neurobiology 20131231 4

The location and morphology of astrocytes are known to contribute to their diversity, and this diversity is often associated with their selective functions. However, molecular markers for astrocyte subtypes are largely unknown. In this study, we found that the immunoreactivity for glycoprotein GPM6B (M6B-IR) is preferentially expressed in the astrocytes associated with ventricles or neurogenic regions of the adult mouse brain. In particular, M6B-IR in the neurogenic niche was confined to glial f ...[more]

PMID: 24465143

Similar Datasets

In vivo reprogramming reactive glia into iPSCs to produce new neurons in the cortex following traumatic brain injury.

Project description:Traumatic brain injury (TBI) results in a significant amount of cell death in the brain. Unfortunately, the adult mammalian brain possesses little regenerative potential following injury and little can be done to reverse the initial brain damage caused by trauma. Reprogramming adult cells to generate induced pluripotent stem cell (iPSCs) has opened new therapeutic opportunities to generate neurons in a non-neurogenic regions in the cortex. In this study we showed that retroviral mediated expression of four transcription factors, Oct4, Sox2, Klf4, and c-Myc, cooperatively reprogrammed reactive glial cells into iPSCs in the adult neocortex following TBI. These iPSCs further differentiated into a large number of neural stem cells, which further differentiated into neurons and glia in situ, and filled up the tissue cavity induced by TBI. The induced neurons showed a typical neuronal morphology with axon and dendrites, and exhibited action potential. Our results report an innovative technology to transform reactive glia into a large number of functional neurons in their natural environment of neocortex without embryo involvement and without the need to grow cells outside the body and then graft them back to the brain. Thus this technology offers hope for personalized regenerative cell therapies for repairing damaged brain.

| S-EPMC4783661 | biostudies-literature

Regenerative neurogenic response from glia requires insulin-driven neuron-glia communication.

Project description:Understanding how injury to the central nervous system induces de novo neurogenesis in animals would help promote regeneration in humans. Regenerative neurogenesis could originate from glia and glial neuron-glia antigen-2 (NG2) may sense injury-induced neuronal signals, but these are unknown. Here, we used Drosophila to search for genes functionally related to the NG2 homologue kon-tiki (kon), and identified Islet Antigen-2 (Ia-2), required in neurons for insulin secretion. Both loss and over-expression of ia-2 induced neural stem cell gene expression, injury increased ia-2 expression and induced ectopic neural stem cells. Using genetic analysis and lineage tracing, we demonstrate that Ia-2 and Kon regulate Drosophila insulin-like peptide 6 (Dilp-6) to induce glial proliferation and neural stem cells from glia. Ectopic neural stem cells can divide, and limited de novo neurogenesis could be traced back to glial cells. Altogether, Ia-2 and Dilp-6 drive a neuron-glia relay that restores glia and reprogrammes glia into neural stem cells for regeneration.

| S-EPMC7880684 | biostudies-literature

GATA3 enhances the neurogenic potential of primary human astrocytes after traumatic injury

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-02-27 | GSE117907 | GEO

ASCL1 reprograms mouse Muller glia into neurogenic retinal progenitors.

Project description:Non-mammalian vertebrates have a robust ability to regenerate injured retinal neurons from Müller glia (MG) that activate the gene encoding the proneural factor Achaete-scute homolog 1 (Ascl1; also known as Mash1 in mammals) and de-differentiate into progenitor cells. By contrast, mammalian MG have a limited regenerative response and fail to upregulate Ascl1 after injury. To test whether ASCL1 could restore neurogenic potential to mammalian MG, we overexpressed ASCL1 in dissociated mouse MG cultures and intact retinal explants. ASCL1-infected MG upregulated retinal progenitor-specific genes and downregulated glial genes. Furthermore, ASCL1 remodeled the chromatin at its targets from a repressive to an active configuration. MG-derived progenitors differentiated into cells that exhibited neuronal morphologies, expressed retinal subtype-specific neuronal markers and displayed neuron-like physiological responses. These results indicate that a single transcription factor, ASCL1, can induce a neurogenic state in mature MG.

| S-EPMC3666387 | biostudies-literature

GATA3 enhances the neurogenic potential of primary human astrocytes after traumatic injury [exp1]

Project description:Astrocytes are an abundant cell type in the vertebrate central nervous system and can act as neural stem cells in specialized niches where they constitutively generate new neurons. Outside the stem cell niches, however, these glial cells are not neurogenic. Although injuries in the mammalian central nervous system lead to profound proliferation of reactive astrocytes (RAs), which cluster at the lesion site to form a gliotic scar, neurogenesis does not take place. Therefore, a plausible regenerative therapeutic option is to coax the RAs to form neurons as an endogenous reservoir for repair. However, little is known on the mechanisms by which regenerative neurogenesis can be induced in mammalian RAs. In zebrafish, Gata acts as a regenerative factor that induces the plasticity of glial cells after injury. However, the effects of GATA in human astrocytes are not known. Therefore, in this report, we investigated how overexpression of GATA in primary fetal human astrocytes would affect the neurogenic potential before and after injury, and determined the transcriptional regulation exerted by GATA using next-generation sequencing. We found that GATA expression in primary human astrocyte cultures is not induced after scratch injury. Lentivirus-mediated overexpression of GATA significantly increased the number of SOX- expressing neural progenitors and altered the expression levels of genes related to cell proliferation and neurogenesis. Our results suggest that GATA is sufficient for enhancing the neurogenic potential of primary human astrocytes after injury.

2019-02-27 | GSE116662 | GEO

GATA3 enhances the neurogenic potential of primary human astrocytes after traumatic injury [exp2]

2019-02-27 | GSE117906 | GEO

Reactive Disruption of the Hippocampal Neurogenic Niche After Induction of Seizures by Injection of Kainic Acid in the Amygdala.

Project description:Adult neurogenesis persists in the adult hippocampus due to the presence of multipotent neural stem cells (NSCs). Hippocampal neurogenesis is involved in a range of cognitive functions and is tightly regulated by neuronal activity. NSCs respond promptly to physiological and pathological stimuli altering their neurogenic and gliogenic potential. In a mouse model of mesial temporal lobe epilepsy (MTLE), seizures triggered by the intrahippocampal injection of the glutamate receptor agonist kainic acid (KA) induce NSCs to convert into reactive NSCs (React-NSCs) which stop producing new neurons and ultimately generate reactive astrocytes thus contributing to the development of hippocampal sclerosis and abolishing neurogenesis. We herein show how seizures triggered by the injection of KA in the amygdala, an alternative model of MTLE which allows parallel experimental manipulation in the dentate gyrus, also trigger the induction of React-NSCs and provoke the disruption of the neurogenic niche resulting in impaired neurogenesis. These results highlight the sensitivity of NSCs to the surrounding neuronal circuit activity and demonstrate that the induction of React-NSCs and the disruption of the neurogenic niche are not due to the direct effect of KA in the hippocampus. These results also suggest that neurogenesis might be lost in the hippocampus of patients with MTLE. Indeed we provide results from human MTLE samples absence of cell proliferation, of neural stem cell-like cells and of neurogenesis.

| S-EPMC6710991 | biostudies-literature

NOTCH1 signaling regulates the latent neurogenic program in adult reactive astrocytes after spinal cord injury.

Project description:Background: Direct reprogramming of astrocytes into neurons opens up a new avenue for neuroregenerative medicine. However, the poor understanding of the molecular mechanisms underpinning the latent neurogenic program in astrocytes has largely restricted this strategy towards safe and effective clinical therapies. Methods: Immunocytochemistry, immunohistochemistry, western blotting, qRT-PCR, gene knockdown and fate-mapping are performed to analyze the role of NOTCH1 signaling in regulation of the latent neurogenic program in reactive astrocytes after spinal cord injury. Results: Western blotting analysis highlights that NOTCH1 is a key signaling mediating Ascl1- and Neurog2-driven astrocyte-to-neuron conversion. Inhibition of NOTCH1 signaling in cultured astrocytes by shRNA or DAPT (a NOTCH1 inhibitor) is sufficient to reprogram them into neurons by upregulating the expression of pro-neural transcription factors, including NeuroD1, NeuroD2, Pax6, Lmx1a and Lhx6. In the spinal cord of adult mouse, the expression of Notch1 is detected in resident astrocytes, which was significantly increased after spinal cord injury (SCI). Genetical knockdown of NOTCH1 signaling alone successfully triggers endogenous reactive astrocytes reprogramming into neurons in the injured adult spinal cord. Importantly, pharmacologically blocking NOTCH1 signaling with small molecule DAPT alone can also induce in situ astrocyte-to-neuron conversion after SCI. Conclusions: We identify NOTCH1 as a key common signaling pathway in reactive astrocyte that provides a barrier for cell fate conversion. This proof-of-principle study will significantly expand our molecular understanding of astroglial-lineage reprogramming and overcoming the NOTCH1 gatekeeper with small molecules may provide a transgene-free approach for in vivo chemical neuronal reprogramming with potential clinical application in neuroregeneration.

| S-EPMC9254256 | biostudies-literature

Berberine protects against neuronal damage via suppression of glia-mediated inflammation in traumatic brain injury.

Project description:Traumatic brain injury (TBI) triggers a series of neuroinflammatory processes that contribute to evolution of neuronal injury. The present study investigated the neuroprotective effects and anti-inflammatory actions of berberine, an isoquinoline alkaloid, in both in vitro and in vivo TBI models. Mice subjected to controlled cortical impact injury were injected with berberine (10 mg·kg(-1)) or vehicle 10 min after injury. In addition to behavioral studies and histology analysis, blood-brain barrier (BBB) permeability and brain water content were determined. Expression of PI3K/Akt and Erk signaling and inflammatory mediators were also analyzed. The protective effect of berberine was also investigated in cultured neurons either subjected to stretch injury or exposed to conditioned media with activated microglia. Berberine significantly attenuated functional deficits and brain damage associated with TBI up to day 28 post-injury. Berberine also reduced neuronal death, apoptosis, BBB permeability, and brain edema at day 1 post-injury. These changes coincided with a marked reduction in leukocyte infiltration, microglial activation, matrix metalloproteinase-9 activity, and expression of inflammatory mediators. Berberine had no effect on Akt or Erk 1/2 phosphorylation. In mixed glial cultures, berberine reduced TLR4/MyD88/NF-κB signaling. Berberine also attenuated neuronal death induced by microglial conditioned media; however, it did not directly protect cultured neurons subjected to stretch injury. Moreover, administration of berberine at 3 h post-injury also reduced TBI-induced neuronal damage, apoptosis and inflammation in vivo. Berberine reduces TBI-induced brain damage by limiting the production of inflammatory mediators by glial cells, rather than by a direct neuroprotective effect.

| S-EPMC4278716 | biostudies-literature

Reactive Balance Responses After Mild Traumatic Brain Injury: A Scoping Review.

Project description:ObjectiveBalance testing after concussion or mild traumatic brain injury (mTBI) can be useful in determining acute and chronic neuromuscular deficits that are unapparent from symptom scores or cognitive testing alone. Current assessments of balance do not comprehensively evaluate all 3 classes of balance: maintaining a posture; voluntary movement; and reactive postural response. Despite the utility of reactive postural responses in predicting fall risk in other balance-impaired populations, the effect of mTBI on reactive postural responses remains unclear. This review sought to (1) examine the extent and range of available research on reactive postural responses in people post-mTBI and (2) determine whether reactive postural responses (balance recovery) are affected by mTBI.DesignScoping review.MethodsStudies were identified using MEDLINE, EMBASE, CINAHL, Cochrane Library, Dissertations and Theses Global, PsycINFO, SportDiscus, and Web of Science. Inclusion criteria were injury classified as mTBI with no confounding central or peripheral nervous system dysfunction beyond those stemming from the mTBI, quantitative measure of reactive postural response, and a discrete, externally driven perturbation was used to test reactive postural response.ResultsA total of 4747 publications were identified, and a total of 3 studies (5 publications) were included in the review.ConclusionThe limited number of studies available on this topic highlights the lack of investigation on reactive postural responses after mTBI. This review provides a new direction for balance assessments after mTBI and recommends incorporating all 3 classes of postural control in future research.

| S-EPMC9339587 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data