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Upregulation of MiR‐122 via Trichostatin A Treatments in Hepatocyte‐like Cells Derived from Mesenchymal Stem Cells
Author(s) -
Alizadeh Effat,
Eslaminejad MohamadReza Baghaban,
Akbarzadeh Abolfazl,
Sadeghi Zohre,
Abasi Mozghan,
Herizchi Roya,
Zarghami Nosratollah
Publication year - 2016
Publication title -
chemical biology and drug design
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.59
H-Index - 77
eISSN - 1747-0285
pISSN - 1747-0277
DOI - 10.1111/cbdd.12664
Subject(s) - downregulation and upregulation , trichostatin a , mesenchymal stem cell , hepatocyte , chemistry , microbiology and biotechnology , mir 122 , hepatocyte nuclear factor 4 , microrna , biology , transcription factor , biochemistry , in vitro , histone deacetylase , histone , gene , nuclear receptor
The miR‐122 is a tissue‐specific mi RNA ; 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 ( HLC s) generated from human adipose tissue‐derived mesenchymal stem cells ( hAT ‐ MSC s). The hepatic differentiation of hAT ‐ MSC s induced by a mixture of growth factors and cytokines either with or without TSA treatments. The functionality of HLC s generated with or without TSA and the expression levels of miR‐122 were studied. The expression levels of miR‐122 in TSA ‐treated HLC s 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 ( LETF s) HNF 4 α (hepatocyte nuclear factor 4 α ) and HNF 6 (hepatocyte nuclear factor 6) were observed in TSA ‐treated HLC s (p < 0.05). In conclusion, administration of TSA in hepatogenic differentiation of hAT ‐ MSC s resulted in higher expression levels of miR‐122, facilitation of differentiation, and subsequently attenuation of AFP levels.