LncRNA NEAT1 Promotes Inflammatory Response in Sepsis via the miR-31-5p/POU2F1 Axis.
Yang YangJianhua XueLili QinJiaxuan ZhangJiajia LiuJunbo YuPublished in: Inflammation (2021)
Sepsis is considered to be a systemic inflammatory response, which results in organ dysfunction. LncRNA nuclear-enriched abundant transcript 1 (NEAT1) involved in sepsis progression has been reported. However, the underlying mechanism of NEAT1 in sepsis-induced inflammatory response remains to be revealed. In this study, NEAT1 and POU domain class 2 transcription factor 1 (POU2F1) were highly expressed in LPS-induced septic RAW264.7 cells, opposite to miR-31-5p expression. Furthermore, we found that NEAT1 silencing inhibited LPS-induced inflammatory response and cell proliferation, and promoted cell apoptosis. Subsequently, we found that miR-31-5p interacted with NEAT1 and targeted the 3'UTR of POU2F1, and in LPS-induced RAW264.7 cells, the inhibition of NEAT1 silencing was reversed by miR-31-5p knockdown, while POU2F1 downregulation could cover the functions of miR-31-5p knockdown. In a word, this study indicates that NEAT1 inhibits the LPS-induced progression of sepsis in RAW264.7 cells by modulating miR-31-5p/POU2F1 axis, suggesting that NEAT1 will be the potential therapeutic target for sepsis.
Keyphrases
- inflammatory response
- lps induced
- acute kidney injury
- lipopolysaccharide induced
- septic shock
- induced apoptosis
- toll like receptor
- intensive care unit
- cell proliferation
- cell cycle arrest
- transcription factor
- signaling pathway
- oxidative stress
- long non coding rna
- poor prognosis
- risk assessment
- endothelial cells
- immune response
- cancer therapy
- climate change