LncRNA NEAT1 promotes the progression of sepsis-induced myocardial cell injury by sponging miR-144-3p

Abstract

Objective: Sepsis is a systemic inflammatory response that can lead to the dysfunction of many organs, including the cardiac one. Long noncoding RNAs (lncRNAs) have been shown to be involved in multiple organ injuries induced by sepsis. However, the regulatory effect of nuclear enriched abundant transcript 1 (NEAT1) on sepsis-induced myocardial injury remains to be explored.

Materials and methods: The sepsis models of myocardial cell injury were constructed using lipopolysaccharide (LPS). Cell counting kit-8 (CCK-8) assay was used to detect cell viability. Flow cytometry was performed to assess cell apoptosis. Moreover, the levels of apoptosis-related and nuclear factor-kappa B (NF-κB) signaling pathway-related proteins were evaluated by Western blot (WB) analysis. Besides, the contents of inflammatory cytokines were tested by enzyme-linked immunosorbent assay (ELISA). The expression levels of NEAT1 and microRNA-144-3p (miR-144-3p) were determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). In addition, Dual-Luciferase reporter and RNA immunoprecipitation (RIP) assays were used to verify the interaction between NEAT1 and miR-144-3p.

Results: LPS could induce myocardial cell injury to construct sepsis models. NEAT1 was upregulated in LPS-treated myocardial cells, and its knockdown promoted viability, suppressed apoptosis, and relieved inflammatory response in LPS-induced myocardial cell injury. MiR-144-3p was downregulated in LPS-treated myocardial cells, and the effect of its overexpression on LPS-induced myocardial cell injury was similar to the effect of NEAT1 knockdown. Besides, miR-144-3p could be sponged by NEAT1, and its inhibitor could reverse the effect of NEAT1 knockdown on LPS-induced myocardial cell injury. Moreover, NEAT1 and miR-144-3p could regulate the activity of NF-κB signaling pathway.

Conclusions: LncRNA NEAT1 could interact with miR-144-3p to regulate sepsis-induced myocardial cell injury through the NF-κB signaling pathway, which might provide a new theoretical basis for the study on the effect of sepsis treatment.