期刊
INFLAMMATION
卷 44, 期 4, 页码 1518-1528出版社
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s10753-021-01436-9
关键词
sepsis; inflammatory response; NEAT1; miR-31-5p
资金
- Science and Technology Project of Nantong City [MS12018057]
NEAT1 inhibits the progression of sepsis induced by LPS in RAW264.7 cells by modulating the miR-31-5p/POU2F1 axis, suggesting NEAT1 as a potential therapeutic target for sepsis.
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.
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