AI Article Synopsis
- Evidence indicates that neuronal microRNAs play a role in synaptic plasticity, but the contribution of glial microRNAs was previously unclear.
- Basic fibroblast growth factor (bFGF) has been shown to increase the expression of miR-134 in astrocytes, with this process linked to specific signaling pathways that can be inhibited.
- Overexpression of miR-134 along with bFGF treatment enhances astrocyte maturation, as evidenced by increased levels of a marker for astrocytes and reduced glutamate levels.
Article Abstract
Evidence suggests that neuronal microRNAs (miRs) contribute to synaptic plasticity, although a role of glial miRs have been unknown. Growth factors including brain-derived neurotrophic factor (BDNF) regulate neuronal functions via upregulation of miRs, while possible influences on expression/function of glial miRs have not been fully understood. Here, we report that basic fibroblast growth factor (bFGF) increased miR-134 expression in astrocyte. The miR-134 was upregulated through stimulating extracellular signal-regulated kinase and phosphatidylinositol 3-kinase signaling, because inhibitors for each signaling blocked the miR-134 induction by bFGF. We also found upregulation of glial fibrillary acidic protein (astrocyte marker) and decreased extracellular concentration of glutamate after miR-134 overexpression and bFGF application, suggesting that astroglial cell maturation is enhanced by bFGF through induction of miR-134.
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| http://dx.doi.org/10.1016/j.bbrc.2014.11.108 | DOI Listing |
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