TK1 and TYMP levels in multiple liver cell lines were assessed along with the cytotoxicity of the thymidine conjugate.
Conclusion: Our quantitative datasets are the first that directly compare multiple human liver cells, define a model for enhanced maintenance of the hepatocyte proteome in culture, and provide a new protein "toolkit" for determining human hepatocyte maturity in cultured cells.
Including multiple human liver cell types can mimic cell cell interactions in specific types of DILI.
Liver regeneration is promoted by multiple types of liver cells, including hepatocytes and liver non-parenchymal cells (NPCs), through complex intercellular signaling.
This proof-of-concept study provided evidence that multiple liver disease-specific cell lines can be generated and that hepatocytes differentiated from these hiPSCs may be useful for modelling liver diseases in vitro and in a patient-specific manner.
For example, hepatocyte-specific autophagic inhibition in Alb-Cre mice resulted in multiple liver tumors, while dendritic cell-specific autophagic inhibition in CD11c-Cre mice exhibited antigen presentation dysfunction [ 10, 39].
Studies have demonstrated that alcohol can impair the functions of proteins in cellular membranes and lipid rafts in liver cells in multiple ways, including actions on lipid-raft associated signalipid-raft associatedd Pruett 2006; Dolganiuc et al. 2006).
First, the findings of the multiple mechanisms of liver cell protection induced by A2aR activation strongly enforce the idea to translate A2aR agonists to the clinical practise as hepatoprotective tool.
Such liver regeneration involves replication of mature parenchyma and non-parenchyma liver cells, which requires multiple cytokine and growth factor signalling pathways, including tumour necrosis factor-alpha, interleukin-6, hepatocyte growth factor (HGF), and transforming growth factor-alpha [ 8, 9].
In mesenchymal cells, transcriptome profiling demonstrated increased expression of multiple liver TISC markers.
