ArticleFrontiers in cellular neuroscience2026
NRG1β-overexpressing mesenchymal stem cell-derived exosomes alleviate oxygen-glucose deprivation-mediated neuronal injury via the miR-296-3p/MAOA axis.
Article in Frontiers in cellular neuroscience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Cerebral ischemic injury is a severe neurological disorder necessitating effective therapeutic strategies. Neuregulin-1β (NRG1β) and microRNAs are critical for neuroprotection, but the mechanisms by which NRG1β regulates microRNAs in neuronal injury are not fully understood. Methods: We characterized mesenchymal stem cells (MSCs) through their phenotypic markers and multilineage differentiation potential, confirming NRG1β overexpression in engineered MSCs. Transmission electron microscopy and nanoparticle tracking analysis were used to isolate and characterize exosomes. Results: Mesenchymal stem cells/NRG1β-exosomes significantly enhanced HT-22 neuronal survival while reducing apoptosis and reactive oxygen species (ROS). The treatment reduced oxidative stress by lowering malondialdehyde (MDA) levels and boosting superoxide dismutase (SOD) activity. It also inhibited inflammatory cytokines such as IL-1β, TNF-α, and IL-6. Studies conducted Conclusion: Our findings demonstrate that exosomes derived from NRG1β-overexpressing mesenchymal stem cells (MSCs) exert neuroprotective effects against ischemic injury by upregulating miR-296-3p. This microRNA targets MAOA, leading to a reduction in apoptosis, oxidative stress, and inflammation. These results highlight the therapeutic potential of MSC/NRG1β-exosomes and the miR-296-3p/MAOA signaling axis in the treatment of ischemic brain injury.
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