Browsing by Subject "Neuronal apoptosis"

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    Exosomes derived from endothelial progenitor cells ameliorate glyoxylate deprivation (OGD)-induced neuronal apoptosis by delivering miR-221-3p
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2023) Pan, Jie; Wu, Tingting; Chen, Bo; Wu, Huadong
    This study evaluated the potential of endothelial progenitor cell (EPC)-derived exosomes as a therapeutic factor for neuronal apoptosis. Mouse EPCs were cultured in vitro, and exosomes were isolated and identified using transmission electron microscopy (TEM), particle size analysis and by determining the protein expressions of exosome markers (CD9, CD63 and Alix). The apoptotic rate of OGD-treated neurons was detected by Flow cytometry assay. The mRNA and protein expression levels were detected by RT-PCR and Western blot assay, respectively. Luciferase reporter assays determined the interaction between miR-221-3p and Bcl2l11. The results showed that most exosomes are 80-120 nm in diameter. Western blot assay showed that CD9, CD63 and Alix were enriched in exosomes. EPCderived exosomes ameliorated OGD-induced neuronal apoptosis. Mechanistically, miR-221-3p from EPCderived exosomes decreased the expression of bcl2l11 in OGD-induced neuronal apoptosis. Moreover, exosomes from miR-221-3p mimics transfected EPCs reduced OGD-induced neuronal apoptosis. In conclusion, miR221-3p in EPC derived exosomes ameliorates OGDinduced neuronal apoptosis, which establish its potential as a new therapeutic method for patients with cerebrovascular diseases.
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    Transcription factors in brain injury
    (Murcia : F. Hernández, 1997) Pennypacker, K.
    After brain injury, neuronal genes are regulated to adjust to an altered environment; however, if neurons are damaged then genes related apoptosis are activated. Glial cells, astrocytes and microglia, respond to neuronal death by transcribing genes to enhance the survival of remaining neurons and for regeneration and repair. AP-1 transcription factors are induced in the neuronal response to injury. Depending on the AP-1 dimer combination, neuronal genes related to either apoptosis or survival are transcribed. A 35 kDa Fosrelated antigen:JunD dimer is present in neurons that survive injury. Jun and JunD exists in neurons prior to undergoing apoptosis. Neuronal death activates gene expression in astrocytes and microglia. NFkB transcription factors are induced in astrocytes reacting to neuronal injury. In the microglial response, STATs appear to be activated to regulate gene transcription. These transcription factors that modulate the genes involved in the cellular processes of brain injury are examined in this review.