ArticleAlcoholism, clinical and experimental research2022
Gag-like proteins: Novel mediators of prenatal alcohol exposure in neural development.
Article in Alcoholism, clinical and experimental research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 19 citations in OpenAlex.
- Maternal microRNAs linked to birth deficits due to prenatal alcohol exposure are dominant modifiers of gene expression in invasive trophoblast cells.Frontiers in cell and developmental biology · 2026Article
- Article
- Sex and age effects on gray matter volume trajectories in young children with prenatal alcohol exposure.Frontiers in human neuroscience · 2024Article
- Sex differences in the transcriptome of extracellular vesicles secreted by fetal neural stem cells and effects of chronic alcohol exposure.Biology of sex differences · 2023Article
- Microbiota and nutrition as risk and resiliency factors following prenatal alcohol exposure.Frontiers in neuroscience · 2023Review
- Article
- Gag-like proteins: Novel mediators of prenatal alcohol exposure in neural development.Alcoholism, clinical and experimental research · 2022Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundWe previously showed that ethanol did not kill fetal neural stem cells (NSCs), but that their numbers nevertheless are decreased due to aberrant maturation and loss of self-renewal. To identify mechanisms that mediate this loss of NSCs, we focused on a family of Gag-like proteins (GLPs), derived from retroviral gene remnants within mammalian genomes. GLPs are important for fetal development, though their role in brain development is virtually unexplored. Moreover, GLPs may be transferred between cells in extracellular vesicles (EVs) and thereby transfer environmental adaptations between cells. We hypothesized that GLPs may mediate some effects of ethanol in NSCs.
methodsSex-segregated male and female fetal murine cortical NSCs, cultured ex vivo as nonadherent neurospheres, were exposed to a dose range of ethanol and to mitogen-withdrawal-induced differentiation. We used siRNAs to assess the effects of NSC-expressed GLP knockdown on growth, survival, and maturation and in silico GLP knockout, in an in vivo single-cell RNA-sequencing dataset, to identify GLP-mediated developmental pathways that were also ethanol-sensitive.
resultsPEG10 isoform-1, isoform-2, and PNMA2 were identified as dominant GLP species in both NSCs and their EVs. Ethanol-exposed NSCs exhibited significantly elevated PEG10 isoform-2 and PNMA2 protein during differentiation. Both PEG10 and PNMA2 were mediated apoptosis resistance and additionally, PEG10 promoted neuronal and astrocyte lineage maturation. Neither GLP influenced metabolism nor cell cycle in NSCs. Virtual PEG10 and PNMA2 knockout identified gene transcription regulation and ubiquitin-ligation processes as candidate mediators of GLP-linked prenatal alcohol effects.
conclusionsCollectively, GLPs present in NSCs and their EVs may confer apoptosis resistance within the NSC niche and contribute to the abnormal maturation induced by ethanol.
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