PUBLICATION

Multi-omics analyses of early liver injury reveals cell-type-specific transcriptional and epigenomic shift

Authors
Migdał, M., Tralle, E., Nahia, K.A., Bugajski, Ł., Kędzierska, K.Z., Garbicz, F., Piwocka, K., Winata, C.L., Pawlak, M.
ID
ZDB-PUB-211221-16
Date
2021
Source
BMC Genomics   22: 904 (Journal)
Registered Authors
Abu Nahia, Karim, Pawlak, Michal, Tralle, Eugeniusz, Winata, Cecilia Lanny
Keywords
ATAC-seq, Chromatin, Endothelial cells, Epigenomics, Genomics, Hepatocytes, Liver, RNA-seq, Stellate cells, Transcriptomics, Zebrafish
Datasets
GEO:GSE145565, GEO:GSE145563, GEO:GSE145564
MeSH Terms
  • Animals
  • Endothelial Cells*
  • Epigenomics*
  • Liver
  • Zebrafish/genetics
PubMed
34920711 Full text @ BMC Genomics
Abstract
Liver fibrosis is a wound-healing response to tissue injury and inflammation hallmarked by the extracellular matrix (ECM) protein deposition in the liver parenchyma and tissue remodelling. Different cell types of the liver are known to play distinct roles in liver injury response. Hepatocytes and liver endothelial cells receive molecular signals indicating tissue injury and activate hepatic stellate cells which produce ECM proteins upon their activation. Despite the growing knowledge on the molecular mechanism underlying hepatic fibrosis in general, the cell-type-specific gene regulatory network associated with the initial response to hepatotoxic injury is still poorly characterized.
In this study, we used thioacetamide (TAA) to induce hepatic injury in adult zebrafish. We isolated three major liver cell types - hepatocytes, endothelial cells and hepatic stellate cells - and identified cell-type-specific chromatin accessibility and transcriptional changes in an early stage of liver injury. We found that TAA induced transcriptional shifts in all three cell types hallmarked by significant alterations in the expression of genes related to fatty acid and carbohydrate metabolism, as well as immune response-associated and vascular-specific genes. Interestingly, liver endothelial cells exhibit the most pronounced response to liver injury at the transcriptome and chromatin level, hallmarked by the loss of their angiogenic phenotype.
Our results uncovered cell-type-specific transcriptome and epigenome responses to early stage liver injury, which provide valuable insights into understanding the molecular mechanism implicated in the early response of the liver to pro-fibrotic signals.
Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping