ArticleMolecular neurobiology2025
Brain-Derived Neurotrophic Factor and Heat Shock Protein-32: Potential Targets for Microglial Response to Glucose and Oxygen Manipulation.
Article in Molecular neurobiology, 2025. 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
Diabetes mellitus-induced mood disorders have physiologically demanding outcomes. Despite the severe outcomes of these comorbidities, the pathogenic mechanisms remain unclear. Hyperglycemia and hypoxia are key features of these conditions. Research indicates that brain-derived neurotrophic factor (BDNF), mainly secreted by microglial cells in response to neuronal stress, plays a role. Encephalic heat shock proteins (HSPs) may protect neurons by preventing death and promoting survival. Therefore, this study investigates (i) the effects of increased glucose concentrations (IGCs) on BDNF expression, (ii) the effects of hypoxia on BDNF expression, (iii) the combined effects of IGCs and hypoxia on BDNF expression, and (iv) the expression of HSPs-27, -32, and -70 under various conditions of IGCs and hypoxia.In-vitro experiments were conducted on Murine BV2 microglial cells to assess cell viability and expression of BDNF and HSPs under different conditions. These included IGCs of 30-, 60-, 90-, 120-mM glucose, hypoxia, and exposure times of 4-, 8-, and 24-h. Results showed short-term IGCs increased cell viability (p < 0.05), while long-term exposure decreased the viability. Combined IGCs and hypoxia had similar effects, with significant increases followed by decreases over time, and increased BDNF expression suggested a protective role. A significant decrease in pro-BDNF at 90 mM glucose after 8 h (p < 0.0001) was noted. Hypoxia-Inducible Factor 1-alpha (HIF1-α) expression in hypoxia-exposed cells decreased over time. HSP70 decreased significantly between 4 and 24 h (p < 0.05), while HSP32 gene expression increased over time. BDNF expression dynamically responded to IGC and hypoxia, which regulated by HIF-1α, with significant HSP involvement, particularly HSP-32, in the glial cell activation.
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