Long noncoding RNA MIR155HG exerts important effects in the progression of multiple diseases. This study investigated the functions of MIR155HG in
sepsis development. Blood samples were collected from 28 patients with
sepsis and 28 without
sepsis. The murine cardiac muscle cell line (HL-1) and macrophage cell line (RAW 264.7) treated with
lipopolysaccharide (LPS) were used as the in vitro
sepsis models. The levels of MIR155HG, miR-194-5p, and MEF2A were determined using real-time-quantitative polymerase chain reaction. Cell counting kit-8 and
terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assays were used to assess cell viability and apoptosis, respectively. The association between miR-194-5p and MIR155HG or MEF2A was confirmed using a dual-
luciferase reporter assay. The levels of inflammatory
cytokines were detected using
enzyme-linked
immunosorbent assay (ELISA). In this study, we demonstrated that MIR155HG expression was significantly increased in
sepsis blood samples, RAW 264.7, and HL-1 cells treated with LPS. Silencing of MIR155HG promoted cell viability and obstructed cell apoptosis and
inflammation of RAW 264.7 and HL-1 cells treated with LPS. MiR-194-5p depletion abrogated cell viability promotion and suppressive effect on cell apoptosis and
inflammation caused by MIR155HG knockdown. In addition, MIR155HG upregulated MEF2A through interaction with miR-194-5p. Finally, rescue assays indicated that MEF2A overexpression abolished the inhibitory effect on
sepsis progression induced by MIR155HG deletion. In conclusion, MIR155HG promotes
sepsis progression in an in vitro
sepsis model by modulating the miR-194-5p/MEF2A axis. This discovery provides a promising
biomarker for
sepsis therapy.