Upregulation of MiR-122 via Trichostatin A Treatments in Hepatocyte-like Cells Derived from Mesenchymal Stem Cells

The miR‐122 is a tissue‐specific miRNA; its expression is abundant in liver. MiR‐122 upregulation is crucial for differentiation, functionality, and maintenance of differentiated phenotype in hepatocytes. The improving effects of trichostatin A (TSA) on hepatic differentiation have been reported previously. The aim of this study was to determine whether TSA can affect the expression of miR‐122 in hepatocyte‐like cells (HLCs) generated from human adipose tissue‐derived mesenchymal stem cells (hAT‐MSCs). The hepatic differentiation of hAT‐MSCs induced by a mixture of growth factors and cytokines either with or without TSA treatments. The functionality of HLCs generated with or without TSA and the expression levels of miR‐122 were studied. The expression levels of miR‐122 in TSA‐treated HLCs was significantly (p < 0.05) higher than those generated by growth factors and cytokines, only. The downregulation of a‐fetoprotein (AFP) levels but enhanced albumin synthesis (p < 0.05) and upregulation of liver‐enriched transcription factors (LETFs) HNF4α (hepatocyte nuclear factor 4α) and HNF6 (hepatocyte nuclear factor 6) were observed in TSA‐treated HLCs (p < 0.05). In conclusion, administration of TSA in hepatogenic differentiation of hAT‐MSCs resulted in higher expression levels of miR‐122, facilitation of differentiation, and subsequently attenuation of AFP levels. Administration of TSA during hepatic differentiation of adipose tissue derived mesenchymal stem cells (AT‐MSCs) resulted in the facilitation of hepatic differentiation, higher miR‐ 122 expression levels, and subsequently attenuation of AFP expression in hepatocyte like cells.