Long noncoding RNA MIR3142HG accelerates lipopolysaccharide-induced acute lung injury via miR-95-5p/JAK2 axis

Abstract

The study aims to clarify the expression pattern of MIR3142HG in acute lung injury (ALI) and investigate the potential mechanisms for the regulatory role of MIR3142HG in JAK/STAT in ALI. Notably, the ALI patients presented the overexpression of MIR3142HG and JAK2 in their serum samples. Knockdown of MIR3142HG facilitated cell viability but impaired cell apoptosis and inflammatory response via targeting miR-95-5p in lipopolysaccharide (LPS)-treated ALI cells. Overexpression of miR-95-5p promoted cell viability but suppressed apoptosis and inflammatory response via targeting JAK2 in LPS-induced ALI cells. The rescue experiments indicated that inhibition of miR-95-5p could reverse the increased cell viability and promote the inhibited apoptosis and inflammatory response induced by MIR3142HG knockdown in LPS-induced ALI. In conclusion, MIR3142HG is increased in sepsis-induced ALI, and MIR3142HG could accelerate the progression of sepsis-induced ALI through miR-95-5p/JAK2 axis, providing theoretical evidence for MIR3142HG to be a promising target for the therapeutics of ALI.

Keywords: Acute lung injury; JAK2; MIR3142HG; miR-95-5p.