Hypoxia-Induced Glioma-Derived Exosomal miRNA-199a-3p Promotes Ischemic Injury of Peritumoral Neurons by Inhibiting the mTOR Pathway

Figure 5

miRNA-199a-3p in HIGDE aggravated neuronal injury by suppressing the mTOR signaling pathway. (a) Representative protein bands and quantification of pmTOR, mTOR, pS6K, and S6K from primary cultured neurons treated with NHIGDE or HIGDE after or in the absence of OGD. vs. HIGDE+OGD; ^# vs. NHIGDE+OGD. (b) The mRNA level of mTOR in primary cultured neurons was lower when the cells were treated with HIGDE than with NHIGDE; however, the expression of S6K was similar. vs. NHIGDE. (c) After OGD/reperfusion injury, when the cells were treated with PA, the LDH level in primary cultured neurons treated with HIGDE+PA (an mTOR activator) distinctly decreased compared with that in the neurons treated with HIGDE+vehicle, similar to the neurons treated with NHIGDE+vehicle. vs. NHIGDE+vehicle; ^# vs. HIGDE+vehicle. (d) The LDH level of primary cultured neurons treated with HIGDE+Lenti S6K (a downstream effector of mTOR) after OGD also decreased compared with that in neurons treated with HIGDE+Lenti GFP, and was similar to that in neurons treated with NHIGDE+Lenti GFP. vs. NHIGDE+Lenti GFP; ^# vs. HIGDE+Lenti GFP. /group in at least 3 independent experiments.

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