Abstract
Microglial inflammation is characterized by an increase in proinflammatory cytokines and proinflammatory enzyme levels, facilitating inflammation-mediated neuronal apoptosis. Previous studies indicated that both high-mobility group protein B1 (HMGB1) and E26 transformation-specific sequence (ETS) transcription factor-1 (ESE-1) are involved in lipopolysaccharide (LPS)-mediated neuroinflammation. In the present study, we hypothesized that the ESE-1 modulates HMGB1 expression and is thus involved in LPS-mediated microglial inflammation. Moreover, we explored the potential mechanism by which ESE-1 modulates HMGB1 expression. Our study indicated that LPS increased proinflammatory cytokine and proinflammatory enzyme levels via upregulation of HMGB1 expression in BV2 cells. Moreover, LPS treatment increased ESE-1 expression while inhibiting sirt1 expression. Both sirt1 overexpression and si-ESE-1 treatment reversed LPS-induced HMGB1 expression and proinflammatory cytokine and proinflammatory enzyme levels. In addition, ESE-1 was found to be associated with sirt1. Also ESE-1 and sirt1 were found to be enriched with the HMGB1 promoter region. Sirt1 silencing increased the abundance of ESE-1 that occupied the HMGB1 promoter region. The present study indicated that ESE-1 associates with sirt1 to regulate HMGB1 expression, which participates in LPS-mediated inflammation in BV2 cells.
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Lu, Y., Ding, J., Huang, J. et al. ESE-1 mediates lipopolysaccharide-induced BV2 cell inflammation via upregulation of HMGB1 expression. J Biosci 48, 43 (2023). https://doi.org/10.1007/s12038-023-00373-z
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DOI: https://doi.org/10.1007/s12038-023-00373-z