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• W4367049590 abstract "Abstract Background Previous studies have confirmed that acute respiratory distress syndrome (ARDS) is characterized by alveolar hypercoagulation and fibrinolytic inhibition. However, the underlying mechanism remains unclear. Runt-related transcription factor 1 (RUNX1) is a transcription factor expressed in various organs, including lung tissue, and is involved in multiple pathophysiological processes such as inflammation. We hypothesized that RUNX1 participates in regulating the pathogenesis of ARDS, but whether it is involved in alveolar hypercoagulation and fibrinolytic inhibition is unclear. Methods In vivo, we observed the expression of RUNX1 in lung tissue in lipopolysaccharide (LPS)-induced ARDS rats and down-regulated the RUNX1 gene to confirm its regulatory role in alveolar hypercoagulation and fibrinolytic inhibition. In vitro, we measured RUNX1 levels in LPS-stimulated alveolar epithelial cell type II (AEC II) and down-and up-regulated RUNX1 gene in AEC II cells using lentiviral infection technology to determine its regulatory role in cells. Finally, we observed the effect of RUNX1 on the NF-κ B pathway and explored the underlying mechanism of RUNX1. Results RUNX1 expression was significantly increased in lung tissue of LPS-induced ARDS rats. Alveolar hypercoagulation and fibrinolytic inhibition were observed in ARDS rats, as shown by increased expressions of tissue factor (TF) and plasminogen activator inhibitor 1 (PAI-1) in lung tissue. Meanwhile, the NF-κB signaling pathway was also activated. Conditional knockdown of RUNX1 significantly inhibited the NF-κB signaling pathway and downregulated the expressions of TF and PAI-1 in pulmonary tissue in rat ARDS. In vitro, we found that the expressions of RUNX1 in LPS-induced AEC II were significantly increased, with the NF-κB pathway being activated. Up-regulation of the RUNX1 gene further boosted the LPS-induced expressions of TF and PAI-1, and the LPS-induced NF-κB pathway activation as well. Down-regulation of the RUNX1 gene, however, dramatically suppressed TF and PAI-1 expressions and significantly inhibited NF-κB pathway activation, even when compared to those in cells stimulated by LPS alone. Conclusions RUNX1 regulates alveolar hypercoagulation and fibrinolysis inhibition in LPS-induced ARDS. The underlying mechanism of RUNX1 may be associated with NF-KB signaling pathway activation. RUNX1 is expected to be a new target for improving alveolar hypercoagulation and fibrinolytic inhibition in ARDS." @default.
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• W4367049590 date "2023-04-26" @default.
• W4367049590 modified "2023-09-27" @default.
• W4367049590 title "RUNX1 promotes alveolar hypercoagulation and fibrinolytic inhibition in LPS-induced ARDS in rat via NF-κ B pathway" @default.
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• W4367049590 doi "https://doi.org/10.21203/rs.3.rs-2847332/v1" @default.
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