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Chemical induction of hepatocyte revitalization in injured human hepatocytes [RNA-seq 3]

ABSTRACT: Chemical induction of hepatocyte revitalization in injured human hepatocytes [RNA-seq 3]

PROVIDER: PRJNA974869 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24682003_1.fastq.gz	Fastqsanger.gz
	SRR24682003_2.fastq.gz	Fastqsanger.gz
	SRR24682004_1.fastq.gz	Fastqsanger.gz
	SRR24682004_2.fastq.gz	Fastqsanger.gz
	SRR24682005_1.fastq.gz	Fastqsanger.gz

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Chemical induction of hepatocyte revitalization in mouse hepatocytes [RNA-seq 2]

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Chemical induction of hepatocyte revitalization in injured human hepatocytes [RNA-seq 3]

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Chemical induction of hepatocyte revitalization in mouse hepatocytes [RNA-seq 1]

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Chemical induction of hepatocyte revitalization in mouse hepatocytes [RNA-seq 1]

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

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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.

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