Project description:We examined how each chemical contributed to hepatocyte revitalization by removing each component of the 5C induction cocktail individually. We then compared deach chemical contributed to hepatocyte revitalization by removing each component of the 5C induction cocktail individually
Project description:3C cocktail could revitalize human hepatocytes displaying apoptotic and EMT phenotypes induced by TGF-β, and promote hepatocyte proliferation and maintenance
Project description:We then compared whole transcriptome bulk RNA-seq data of dHeps isolated from CCl4-injured mice and treated with either 5C, 3C, or DMSO. The expression of hepatocyte-enriched TFs and hepatocyte functional genes was upregulated in both the 5C and 3C groups, while mesenchymal markers (Acta2, Mmp3), inflammatory-related genes (Cxcl10, Ecm1, Ccl6, and Cd68), and oxidative stress-related genes (Ncf2 and Ncf1), were down-regulated compared with their expression in the DMSO control group
Project description:Gene expression was analyzed and compared of normal mouse hepatocyte, premalignant hepatocytes and fully malignant HCC cells. The results provide valuable information about the gene expression alterations during the chronic process of liver cancer development. HCC in age-matched male mice were induced by DEN injection. Normal mouse hepatocyte, premalignant hepatocytes and fully malignant HCC were freshly isolated and RNA extracted.
Project description:Transcriptional profiling of in vitro cultured mouse hepatocytes and hepatocyte-derived biliary cells demonstrated that in vitro cultured cells recapitulates the major transcriptional features of in vivo biliary cells and hepatocytes.
Project description:The liver has a remarkable capacity for regeneration after injury. Midlobular hepatocytes have been proposed as the most plastic hepatic cell type, providing definitive evidence that zone 2 of the liver lobule acts as a reservoir for hepatocyte proliferation during homeostasis and regeneration. However, the implication of other mechanisms beyond hyperplasia that contribute to liver repair have been little explored and the collaboration of another hepatocyte subpopulation has differed among previous studies depending on the model of liver injury used. Thus, re-examination of dynamics of hepatocytes during regeneration is critical to get a better understanding of underlaying mechanisms for potential cell therapy and treatment of liver diseases. Here, using a mouse model of hepatocyte- and non-hepatocyte-specific multicolor lineage tracing, we demonstrate that hepatocytes located in the midlobular region also undergo hypertrophy besides cell division in response to chemical, physical, and viral insults. Our study shows for first time that this subpopulation also combats liver impairment after infection with coronavirus. Furthermore, we demonstrate that pericentral hepatocyte subpopulation also expands in number and size during the repair process in collaboration with midlobular hepatocytes and Galectin-9-CD44 pathway may be critical for driving these processes. Interestingly, we identified transdifferentiation and cell fusion processes during liver regeneration after severe injury that may be key to recover hepatic function.
Project description:Gene expression was analyzed and compared of normal mouse hepatocyte, premalignant hepatocytes and fully malignant HCC cells. The results provide valuable information about the gene expression alterations during the chronic process of liver cancer development.