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Neural stem and progenitor cells support and protect adult hippocampal function via vascular endothelial growth factor secretion. | LitMetric

AI Article Synopsis

  • Adult neural stem and progenitor cells (NSPCs) in the dentate gyrus (DG) of the hippocampus can not only produce new neurons but also secrete growth factors like vascular endothelial growth factor (VEGF), influencing their environment.
  • Researchers found that the absence of NSPC-derived VEGF led to impaired memory, increased neuronal hyperexcitability, and worsened excitotoxic injury in the hippocampus, highlighting its importance for brain function.
  • Overexpressing VEGF reduced harmful microglial responses during injury, suggesting NSPCs play a crucial role in protecting DG function through VEGF secretion, beyond just generating new neurons.

Article Abstract

Adult neural stem and progenitor cells (NSPCs) reside in the dentate gyrus (DG) of the hippocampus throughout the lifespan of most mammalian species. In addition to generating new neurons, NSPCs may alter their niche via secretion of growth factors and cytokines. We recently showed that adult DG NSPCs secrete vascular endothelial growth factor (VEGF), which is critical for maintaining adult neurogenesis. Here, we asked whether NSPC-derived VEGF alters hippocampal function independent of adult neurogenesis. We found that loss of NSPC-derived VEGF acutely impaired hippocampal memory, caused neuronal hyperexcitability and exacerbated excitotoxic injury. Conversely, we observed that overexpression of VEGF reduced microglial response to excitotoxic injury. We also found that NSPCs generate substantial proportions of total DG VEGF and VEGF disperses widely throughout the DG, both of which help explain how this anatomically-restricted cell population could modulate function broadly. These findings suggest that NSPCs actively support and protect DG function via secreted VEGF, thereby providing a non-neurogenic functional dimension to endogenous NSPCs.

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Source
http://dx.doi.org/10.1038/s41380-024-02827-8DOI Listing

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