Fig. 8: a miR-711 is predominately expressed by neurons in vitro.

miR-711 expression was analyzed by qPCR in primary cultured cortical neurons, microglia, and astrocytes. Neurons were exposed to cell death inducers etoposide (Etop, 25 nM) or staurosporine (Stau, 25 nM) for 6 h, microglia were treated with LPS (30 ng/ml) or IFNγ (60 ng/ml) for 24 h, astrocytes were treated with LPS (1 μg/ml), TGFβ1 (30 ng/ml), or 10% FBS for 24 h. The data are presented as independent data points. One-way ANOVA was conducted followed by Newman-Keuls multiple comparisons test. n = 3–5 dishes/group repeated in three independent cultures. ***p < 0.001, ^###p < 0.001 vs. Control (neurons). b The functional role of miR-711 in regulating neuronal cell death, axonal and blood vessel damage after SCI. SCI-induced elevation of miR-711 can initiate secondary injury pathways including neuronal cell death, axonal damage, and vascular disruption, through in part, inhibition of Akt and Angiopoietin-1 (Ang-1) pathways. Administration of miR-711 inhibitor in the acute period after SCI has significant neuroprotective effects, likely acting both directly on neurons and by limiting Ang-1-mediated vascular permeability effects