Astrocytes protect oligodendrocyte precursor cells via MEK/ERK and PI3K/Akt signaling

Arai, Ken; Lo, Eng H.

doi:10.1002/jnr.22256

Cited by 101Neurogenesis and neuroplasticity mechanismsNeuroinflammation and Neurodegeneration MechanismsNeuroscience and Neuropharmacology Research

Astrocytes protect oligodendrocyte precursor cells via MEK/ERK and PI3K/Akt signaling

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Arai, Ken, Lo, Eng H.·2010·Journal of Neuroscience Research

DOI 10.1002/jnr.22256PMC PMC3705578

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Abstract

Accumulating evidence suggest that trophic coupling among different cell types in the brain is required to maintain normal CNS function. Here we show that astrocytes secrete soluble factors that can be oligodendrocyte‐supportive. Oligodendrocyte precursor cells (OPCs) and astrocytes were prepared from neonatal rat brain and cultured separately. We conducted cell culture medium‐transfer experiments to examine whether astrocytes secrete OPC‐protective factors. Conditioned media from astrocytes protected OPCs against H 2 O 2‐induced oxidative stress, starvation, and oxygen‐glucose deprivation. This protective effect may be mediated in part via ERK and Akt signaling pathways. Astrocyte‐conditioned media upregulated the phosphorylation levels of ERK and Akt in OPC cultures. Blockade of ERK or Akt signaling with U0126 or LY294002 cancelled the OPC‐protective effects of astrocyte‐conditioned media. Taken together, these data suggest that astrocytes are an important source for oligodendrocyte‐supportive factors. Coupling between these two major glial components in brain may be vital for sustaining white matter homeostasis. © 2009 Wiley‐Liss, Inc.

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Vascular oxidative stress and inflammation impede proliferation, migration, and differentiation of oligodendrocyte progenitor cells and compromise repair of damaged white matter.
“Vascular oxidative stress and inflammation impede the proliferation, migration, and differentiation of oligodendrocyte progenitor cells and compromise repair of the damaged white matter.108,132,133”
From Vascular Contributions to Cognitive Impairment and Dementia: A Statement for Healthcare Professionals From the American Heart Association/American Stroke Association (2011) · cites this paper as [132]
The Discussion (page unavailable) reports that cultured rat OPCs were vulnerable to hydrogen-peroxide oxidative stress, and the paper states that OPCs contribute to white-matter repair. It does not show that vascular oxidative stress or inflammation impedes OPC proliferation, migration, or differentiation, or directly demonstrate impaired repair of damaged white matter. (LLM, conf=0.88)
Experimental — accuracy not yet measured
Withdrawal of trophic support from damaged endothelial cells and astrocytes could reduce oligodendrocyte progenitor cell pool vitality and contribute to their demise in hypoxic vulnerable white matter.
“Second, withdrawal of trophic support from damaged endothelial cells and astrocytes could reduce the vitality of the OPC pool and contribute to their demise in the hypoxic environment of the vulnerable white matter (Arai and Lo, 2010).”
From The Pathobiology of Vascular Dementia (2013) · cites this paper as Arai and Lo, 2010

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Authors: Arai, K., & Lo, E. H.
Affiliations: Harvard University (US)
Corresponding author: Arai, Ken
ORCID: Arai, Ken
Lo, Eng H.
Venue: Journal of Neuroscience Research
Publisher: Wiley
Published: 2009-10-14
Volume: 88
Issue: 4
Pages: 758-763
ISSN: 0360-4012 (ISSN-L)
1097-4547
DOI: 10.1002/jnr.22256
PMC: PMC3705578
OpenAlex: W1989903772
Cited by: 101
References: 46
Citations by year: 2025: 2 · 2024: 6 · 2023: 7 · 2022: 5 · 2021: 8 · 2020: 7 · 2019: 3 · 2018: 7 · 2017: 7 · 2016: 5 · 2015: 4 · 2014: 9 · 2013: 9 · 2012: 10
FWCI: 2.30
Type: journal article
Language: en
Open access: green
europepmc.org
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations: Journal of Neuroscience Research (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: National Institutes of Health
National Institute of Neurological Disorders and Stroke (RC2NS069335, P01NS055104)
Topics: Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Keywords: astrocytes, oligodendrocyte precursor cells, trophic support, MEK/ERK signaling, PI3K/Akt signaling, conditioned medium, oxidative stress, oxygen-glucose deprivation, glial interactions
MeSH terms: Chondroitin Sulfate Proteoglycan 4, Animals, Animals, Newborn, Hypoxia, Antigens, Astrocytes, Enzyme Inhibitors, Gangliosides, Glial Fibrillary Acidic Protein, Glucose, Hydrogen Peroxide, Oligodendroglia, Proteoglycans, Stem Cells, Signal Transduction, Culture Media, Serum-Free, Culture Media, Conditioned, Rats, Sprague-Dawley, Oxidative Stress, Phosphatidylinositol 3-Kinases, MAP Kinase Kinase Kinases, Cell Proliferation, Rats

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Astrocytes protect oligodendrocyte precursor cells via MEK/ERK and PI3K/Akt signaling

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