miR-155 Is Essential for Inflammation-Induced Hippocampal Neurogenic Dysfunction.

摘要: Peripheral and CNS inflammation leads to aberrations in developmental postnatal neurogenesis, yet little is known about the mechanism linking neurogenic abnormalities. Specific miRs regulate peripheral inflammatory responses. miR-155 most significantly upregulated miR primary murine microglia stimulated with lipopolysaccharide (LPS), a proinflammatory Toll-Like Receptor 4 ligand. Here, we demonstrate that essential for robust IL6 gene induction under LPS stimulation vitro. LPS-stimulated enhance astrogliogenesis of cocultured neural stem cells (NSCs), whereas blockade or genetic ablation microglial restores differentiation. knock-out mice show reversal LPS-induced deficits activation vivo. Moreover, transgenic elevated expression nestin-positive hematopoietic cells, including microglia, increased cell proliferation ectopically localized doublecortin-positive immature neurons radial glia-like hippocampal dentate gyrus (DG) granular layer. Microglia have proliferative effects on NSCs, which are altered by overexpression. In addition, elevation numbers amoeboid morphology DG. Our study demonstrates inflammation-induced via sufficient disrupting normal development.