MiR‑155 mediates inflammatory injury of hippocampal neuronal cells via the activation of microglia.

Abstract

MicroRNA (miR)-155 has a crucial role in various cellular functions, including differentiation of hematopoietic cells, immunization, inflammation and cardiovascular diseases. The present study aimed to investigate the roles and mechanisms of miR-155 in treatment-resistant depression (TRD). A Cell Counting Kit-8 assay and flow cytometry were performed to assess the cell viability and apoptosis of microglial cells, respectively. Western blotting and reverse transcription-quantitative polymerase chain reaction assays were used to evaluate the associated protein and mRNA expression, respectively. The results revealed that miR-155 reduced the cell viability of BV-2 microglial cells, and miR-155 enhanced the expression levels of pro-inflammatory cytokines in BV-2 microglial cells. Furthermore, conditioned medium from miR-155-treated microglia decreased the cell viability of HT22 hippocampal cells. miR-155-treated microglia increased the apoptosis of neuronal hippocampal cells by modulating the expression levels of apoptosis regulator Bax, apoptosis regulator Bcl-2, pro-caspase-3 and cleaved-caspase-3. The cell cycle distribution was disrupted by miR-155-treated microglia through induction of S phase arrest. Furthermore, the overexpression of suppressor of cytokine signaling 1 reversed the pro-apoptotic effect of activated microglia on hippocampal neuronal cells. In conclusion, the present results suggested that miR-155 mediated the inflammatory injury in hippocampal neuronal cells by activating the microglial cells. The potential effects of miR-155 on the activation of microglial cells suggest that miR-155 may be an effective target for TRD therapies.