Methylome variation after TSA treatment of equine chondrocyte cell lines
One of the usable regenerative approaches in cartilage defects is to obtain cartilage cells from the healthy surfaces of the joints, and their in vitro expansion before chondrocyte implantation in places of damaged cartilage. In order to diminish the chondrocyte phenotypic loss during in vitro expansion a range of biological stimulants has been tested until now including such able to alter epigenetic modifications of regulatory elements of genes like methylation of DNA. One of the common epigenetic modifiers is Trichostatin A (TSA) - an inhibitor of histone deacetylases (HDAC) silencing gene transcription through chromatin condensation. The aim of study was TSA influence on variability of DNA methylation in the genomes of expanded equine chondrocytes in monolayer culture. The RRBS approach was used to reveal the sites of differential methylation in genomes of TSA treated and untreated chondrocytes expanded until the third passage. As the result many of differentially methylated sites were found in loci of genes involved in the canonical pathways and biological processes important for the biology and pathology of hard connective tissue, underscoring the role of epigenetic TSA stimulation of expanded cells.