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HIV-1 Tat induced microglial EVs leads to neuronal synaptodendritic injury: microglia-neuron cross-talk in NeuroHIV

Figure 3. Role of BV2 derived exosomes from BV2 on neuronal synaptic proteins. (A) Schematic representation showing the exposure of BV2-derived exosomes to primary neurons. Representative western blot images and their quantitative analysis showing the dose-dependent effects of BV2-derived exosomes on the expression of (B) PSD95, (C) GAD65, and (D) Gephyrin in rat cortical primary neurons. (E) Representative western blot images and quantitative analysis showing the expression of NLRP3 in BV2 cells transfected with either NLRP3 or scrambled siRNA in the presence of Tat (50 ng/mL) to confirm the transfection efficiency of NLRP3. Representative western blots and their quantitative analysis showing the expression of (F) PSD95, (G) GAD65, and (H) Gephyrin in rat primary cortical neurons exposed with MDEVs from NLRP3 siRNA transfected BV2 cells in the presence of Tat (50 ng/mL). β-actin was used as a loading control. Data are presented as mean ± SEM. *P < 0.05 vs. siControl MDEV, #P < 0.05 vs. Tat MDEV. One-way ANOVA followed the Bonferroni post hoc tests were used for statistical analysis. MDEV: Microglia derived exosomes’ HT: heated Tat; NLRP3: NOD-, LRR- and pyrin domain-containing protein 3; PSD95: postsynaptic density protein 95; GAD65: glutamic acid decarboxylase; siRNA: small interfering RNA; Tat: trans-activator of transcription.

Extracellular Vesicles and Circulating Nucleic Acids
ISSN 2767-6641 (Online)
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