ArticleBulletin of experimental biology and medicine2021
Role of MAPK ERK1/2 and p38 in the Regulation of Secretory Functions of Different Populations of Neuroglia in Ethanol-Induced Neurodegeneration.
Article in Bulletin of experimental biology and medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- Roles of Oxidative Stress and Autophagy in Alcohol-Mediated Brain Damage.Antioxidants (Basel, Switzerland) · 2025Review
- Alcoholic brain injury is a modifiable risk factor: natural active substance intervention promises to improve alcohol-induced cognitive impairment.Frontiers in nutrition · 2025Review
- Investigation of Uncovering Molecular Mechanisms of Alcohol-Induced Female Infertility-A Rational Approach.Reproductive sciences (Thousand Oaks, Calif.) · 2024Review
- Functional State of Various Types of Regenerative-Competent Neural Tissue Cells in β-Amyloid-Induced Neurodegeneration.Bulletin of experimental biology and medicine · 2022Article
- The Role of MARK ERK1/2 and p38 in Regulation of Functions of Neural Stem Cells and Neuroglia under Conditions of β-Amyloid-Induced Neurodegeneration.Bulletin of experimental biology and medicine · 2022Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
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Abstract
We studied the participation of ERK1/2 and p38 in secretion of neurotrophic growth factors by various types of neuroglia under conditions of in vitro and in vivo modeled ethanol-induced neurodegeneration. The inhibitory role of these protein kinases in the production of neurotrophins by intact astrocytes and the absence of their participation in the regulation of functions of oligodendrocytes and microglial cells were shown. Under conditions of ethanol neurotoxicity, the role of ERK1/2 and p38 in the production of growth factors by glial elements was significantly changed. Neurodegeneration modeled in vitro led to inversion of the role of both protein kinases in the secretion of neurotrophins by astroglia and inhibition of the cytokine-synthesizing function of oligodendrocytes and microglial cells by ERK1/2 and p38. In mice receiving ethanol per os for a long time (as well as in cells in vitro exposed to ethanol), mitogen-activated kinases stimulated the function of astrocytes and inhibited the production of growth factors by microglial cells. At the same time, chronic alcoholization was accompanied by the appearance of the stimulating role of ERK1/2 and p38 in the implementation of the secretory function by oligodendrocytes.
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