Abstract
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.
Highlights
Sepsis is a systemic inflammatory response syndrome (SIRS) resulting from infection [1], which often occurs in patients with severe burns, trauma, and surgery
We firstly detected the content of inflammatory cytokines by QPCR and ELISA assay and the data showed that LPS significantly upregulated the level of TNF-α, IL-6, and IL-1β in RAW 264.7 cells, while sh-nuclear-enriched abundant transcript 1 (NEAT1) reversed these effects of LPS on inflammatory cytokines (Fig. 2a, b)
Afterwards, EDU staining was performed and the results illustrated that knockdown of NEAT1 clearly increased the percentage of EDU-positive signals in LPS-induced RAW264.7 cells (Fig. 2d), suggesting that NEAT1 was involved in the RAW264.7 cell proliferation
Summary
Sepsis is a systemic inflammatory response syndrome (SIRS) resulting from infection [1], which often occurs in patients with severe burns, trauma, and surgery. NEAT1 in circulating blood is associated with increased disease risk, ascending severity of the disease, poor prognosis, and rising expression of inflammatory factors in sepsis patients [16], and Chen et al.’s study shows that NEAT1 is highly expressing in patients with sepsis, and aggravates LPSinduced cell injury via regulating miR-204/NF-κB axis [17], suggesting that NEAT1 has a significant proinflammatory effect. These studies suggest that NEAT1 is closely related to sepsis-induced inflammatory response, the specific mechanism of NEAT1 in sepsis progression is still worth investigating
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