ABSTRACT
The aim of the present study was to investigate whether long noncoding RNA metastasis associated lung adenocarcinoma transcript 1 (MALAT1) could modulate activation and inflammation of hepatic stellate cell (HSCs) via regulation of a microRNA (miR)181atoll like receptor (TLR)4/nuclear factor (NF)κB axis, thereby contributing to the development of liver fibrosis. A total of 151 patients with liver fibrosis were recruited, and the serum levels of alanine transaminase, aspartate aminotransferase and albumin were determined. Transforming growth factor (TGF)ß1 and LPS were used to activate and induce inflammation in the human HSC cell line LX2. MALAT1 was knocked using small interfering RNA or overexpressed, and an inhibitor and mimic of miR181a5p were used to examine the effect of MALAT1 and miR181a5p on the activation and inflammation of LX2 cells. Both MALAT1 and miR181a5p expression performed well in their ability to differentiate patients with liver fibrosis from healthy volunteers, and MALAT1 expression was associated with the severity of liver fibrosis. The expression levels of TLR4 and NFκB were increased after stimulation with LPS or TGFß1, but MALAT1 knockdown or miR181a5p mimic transfection abrogated this increase. Moreover, the TGFß1induced increase in viability, proliferation, migration, adhesion and collagen production, and the LPSinduced inflammation of LX2 cells were all reversed after MALAT1 knockdown or transfection with miR181a5p mimic. The MALAT1/miR181a5p axis was involved in regulating collagen production and inflammation by activating TLR4/NFκB signaling, which may be conducive to liver fibrosis treatment in the future.