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Expression of pluripotency‐related genes is highly dependent on trichostatin A‐assisted epigenomic modulation of porcine mesenchymal stem cells analysed for apoptosis and subsequently used for generating cloned embryos
Author(s) -
Samiec Marcin,
Romanek Joanna,
Lipiński Daniel,
Opiela Jolanta
Publication year - 2019
Publication title -
animal science journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.606
H-Index - 38
eISSN - 1740-0929
pISSN - 1344-3941
DOI - 10.1111/asj.13260
Subject(s) - homeobox protein nanog , sox2 , trichostatin a , rex1 , biology , mesenchymal stem cell , microbiology and biotechnology , stem cell , embryonic stem cell , induced pluripotent stem cell , histone deacetylase , histone , genetics , gene
The present study sought to examine whether trichostatin A (TSA)‐assisted epigenetic transformation of porcine bone marrow (BM)‐derived mesenchymal stem cells (BM‐MSCs) affects the transcriptional activities of pluripotency‐related genes ( Oct4 , Nanog , c‐Myc , Sox2 and Rex1 ), multipotent stemness‐related gene ( Nestin ) and anti‐apoptotic/anti‐senescence‐related gene ( Survivin ). Epigenetically transformed or non‐transformed BM‐MSCs that had been transcriptionally profiled by qRT‐PCR and had been analysed for different stages of apoptosis progression provided a source of nuclear donor cells for the in vitro production of cloned pig embryos. TSA‐mediated epigenomic modulation has been found to enhance the multipotency extent, stemness and intracellular anti‐ageing properties of porcine BM‐MSCs. This has been confirmed by the relative abundances for Nanog , c‐Myc Rex1 , Sox2 and Survivin mRNAs in TSA‐exposed BM‐MSCs that turned out to be significantly higher than those of TSA‐unexposed BM‐MSCs. Additionally, TSA‐assisted epigenomic modulation of BM‐MSCs did not impact the caspase‐8 activity, Bax protein expression and the incidence of TUNEL‐positive cells. In conclusion, the considerably elevated quantitative profiles of Sox2 , Rex1 , c‐Myc , Nanog and Survivin mRNA transcripts seem to trigger improved reprogrammability of TSA‐treated BM‐MSC nuclei in cloned pig embryos that thereby displayed remarkably increased blastocyst formation rates as compared to those noticed for embryos derived from TSA‐untreated BM‐MSCs.

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