The Modulatory Role of Endogenous IL-24/mda-7 in Inflammatory Response of Human Hepatic Stellate Cell (HSC), LX2

High morbidity and limited therapies of hepatic fibro genesis are important factor for better understanding the molecular mechanisms of the disease. Advances in the understanding of the molecular behavior of hepatic stellate cells (HSC) allow the progress of a field dedicated to anti-fibrotic therapy. Melanoma differentiation associated gene-7 (IL-24/mda-7) as a gene induced during terminal differentiation in human melanoma cells, but the inflammatory response of cells to IL-24/mda-7 is not entirely cleared.
Materias and LX-2 cells (a human hepatic stellate cell) were treated by leptin (positive control), media (control negative), or were transfected by empty plasmid and pcDNA3.1/mda-7. The inflammatory state was evaluated through measuring the mRNA expression level of inflammatory molecule, IL-1β. The role of IL-24/mda-7 modulation on inflammatory response was assayed using SOCS1 and SOCS3 gene expressions.
The expression levels of IL-1β, SOCS1 and SOCS3 were compared in LX-2 cell line groups. The expression of the IL-1β in the transfected cells was higher than the control cell, but it was not significant. The results indicated that the expressions of SOCS1 and SOCS3 were up-regulated following pcDNA 3.1/mda-7 transfection into LX-2 cells compared to control plasmids (p=0.0179, p=0.0428).
The endogenous IL-24/mda-7 exhibited a significant modulatory effect on stellate cells. Therefore, IL-24/mda-7 and relevant signaling pathways could be employed as a target for fibrosis treatment.