ArticleMolecular neurobiology2016
Inflammation Promotes a Conversion of Astrocytes into Neural Progenitor Cells via NF-κB Activation.
Article in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
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Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.
- The core of maintaining neuropathic pain: Crosstalk between glial cells and neurons (neural cell crosstalk at spinal cord).Brain and behavior · 2023Pooled it
- Co-Delivery of Sustained Release Chondroitinase ABC-37 With Human iPSC-Derived Neural Progenitors Promotes Transplant Survival and Functional Recovery in a Rodent Model of Stroke.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Connexin Regulation and Modulation of Neural Stem Cell Differentiation Induced by Cell-Permeable Itaconate.Journal of cellular physiology · 2026Article
- Hcfc1 and Ogt Mediate Zebrafish CNS Regeneration Through Hippo/Yap Signalling.Cell proliferation · 2026Article
- Antiretroviral drug therapy does not reduce neuroinflammation in an HIV-1 infection brain organoid model.Journal of neuroinflammation · 2025Article
- Traumatic brain injury promotes neurogenesis at the cost of astrogliogenesis in the adult hippocampus of male mice.Nature communications · 2024Article
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- BCAS1 defines a heterogeneous cell population in diffuse gliomas.Oncotarget · 2024Article
- Efficient derivation of functional astrocytes from human induced pluripotent stem cells (hiPSCs).PloS one · 2024Article
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- Glial progenitor heterogeneity and key regulators revealed by single-cell RNA sequencing provide insight to regeneration in spinal cord injury.Cell reports · 2023Article
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- MYC promotes fibroblast osteogenesis by regulating ALP and BMP2 to participate in ectopic ossification of ankylosing spondylitis.Arthritis research & therapy · 2023Article
- Protein kinase B (AKT) upregulation and Thy-1-αJournal of neuroinflammation · 2023Article
- Endotype Characterization Reveals Mechanistic Differences Across Brain Regions in Sporadic Alzheimer's Disease.Journal of Alzheimer's disease reports · 2023Article
- Dedifferentiation andMolecular medicine reports · 2022Review
- Cornuside Is a Potential Agent against Alzheimer's Disease via Orchestration of Reactive Astrocytes.Nutrients · 2022Article
- Enriching neural stem cell and anti-inflammatory glial phenotypes with electrical stimulation after traumatic brain injury in male rats.Journal of neuroscience research · 2021Article
- Astrocytes in Multiple Sclerosis-Essential Constituents with Diverse Multifaceted Functions.International journal of molecular sciences · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Brain inflammation, a common feature in neurodegenerative diseases, is a complex series of events, which can be detrimental and even lead to neuronal death. Nonetheless, several studies suggest that inflammatory signals are also positively influencing neural cell proliferation, survival, migration, and differentiation. Recently, correlative studies suggested that astrocytes are able to dedifferentiate upon injury and may thereby re-acquire neural stem cell (NSC) potential. However, the mechanism underlying this dedifferentiation process upon injury remains unclear. Here, we report that during the early response of reactive gliosis, inflammation induces a conversion of mature astrocytes into neural progenitors. A TNF treatment induces the decrease of specific astrocyte markers, such as glial fibrillary acidic protein (GFAP) or genes related to glycogen metabolism, while a subset of these cells re-expresses immaturity markers, such as CD44, Musashi-1, and Oct4. Thus, TNF treatment results in the appearance of cells that exhibit a neural progenitor phenotype and are able to proliferate and differentiate into neurons and/or astrocytes. This dedifferentiation process is maintained as long as TNF is present in the culture medium. In addition, we highlight a role for Oct4 in this process, since the TNF-induced dedifferentiation can be prevented by inhibiting Oct4 expression. Our results show that activation of the NF-κB pathway through TNF plays an important role in the dedifferentiation of astrocytes via the re-expression of Oct4. These findings indicate that the first step of reactive gliosis is in fact a dedifferentiation process of resident astrocytes mediated by the NF-κB pathway.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.