a20 attenuates lipopolysaccharide-induced inflammation through mapk/erk/jnk pathway in lx-2 cells

Background: hepatic stellate cells (hscs) are liver-specific pericytes that transform into myofibroblasts, which are involved in pathological vascularization in liver fibrosis. we previously suggested that a20 overexpression suppresses lipopolysaccharide (lps)-induced inflammation in hsc. we aimed to determine the mechanisms of the anti-inflammatory role of a20 in lx-2 cells. methods: lx-2 cells were transfected with a20-sirna or control-sirna and control adenovirus or a20-carrying adenovirus. quantitative reverse transcription pcr (rt-qpcr) analysis was employed to quantify mrna levels of α-sma, col-i, col-iii, il-6, tgf-β, and pdgf in a20-sirna lx-2 cells stimulated with lps. multiple molecular indices of mapk/erk/jnk signal pathway were performed by using western blotting. results: relative to control, the fibrosis-related mrna levels of α-sma, col-i, and col-iii were increased in a20-sirna lx-2 cells. meanwhile, a20-sirna cells significantly increased il-6, tgf-β, and pdgf mrna levels. relative to controls, stimulating a20 overexpressing lx-2 cells with lps for 5 and 30 minutes significantly reduced the levels of phosphorylated erk and jnk, respectively. a20 knockdown in lx-2 cells promotes phosphorylated erk and jnk levels with lps for 30 minutes. conclusions: our data indicate that a20 could be functional in hscs through the mapk/erk/jnk signaling pathway, highlighting a potential novel therapeutic strategy against liver fibrosis.