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Co-culture with mouse embryonic fibroblasts improves maintenance of metabolic function of human small hepatocyte progenitor cells

ABSTRACT: Co-culture with mouse embryonic fibroblasts improves maintenance of metabolic function of human small hepatocyte progenitor cells

PROVIDER: PRJNA662788 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12622079.fastq.gz	Fastqsanger.gz
	SRR12622080.fastq.gz	Fastqsanger.gz
	SRR12622081.fastq.gz	Fastqsanger.gz
	SRR12622082.fastq.gz	Fastqsanger.gz
	SRR12622083.fastq.gz	Fastqsanger.gz

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Co-culture with mouse embryonic fibroblasts improves maintenance of metabolic function of human small hepatocyte progenitor cells

Project description:Small hepatocyte progenitor cells (SHPCs) can be derived from primary adult human hepatocytes on mouse embryonic fibroblasts (MEFs). SHPCs derived and cultured on MEFs retain their differentiated morphology and gene expression profiles over several passages. SHPCs in MEF co-culture metabolize acetaminophen to all of its major metabolites at rates equal to mature adult primary human hepatocytes.

2020-09-11 | GSE157791 | GEO

Co-culture with mouse embryonic fibroblasts improves maintenance of metabolic function of human small hepatocyte progenitor cells.

Project description:Derivation and culture of small hepatocyte progenitor cells (SHPCs) capable of proliferating in vitro has been described in rodents and recently in humans. These cells are capable of engrafting in injured livers, however, they display de-differentiated morphology and reduced xenobiotic metabolism activity in culture over passages. Here we report that SHPCs derived from adult primary human hepatocytes (PHHs) and cultured on mouse embryonic fibroblasts (MEFs) not only display differentiated morphology and exhibit gene expression profiles similar to adult PHHs, but importantly, they retain their phenotype over several passages. Further, unlike previous reports, where extensive manipulations of culture conditions are required to convert SHPCs to metabolically functional hepatocytes, SHPCs in our co-culture system maintain expression of xenobiotic metabolism-associated genes. We show that SHPCs in co-culture are able to perform xenobiotic metabolism at rates equal to their parent PHHs as evidenced by the metabolism of acetaminophen to all of its major metabolites. In summary, we present an improved co-culture system that allows generation of SHPCs from adult PHHs that maintain their differentiated phenotype over multiple passages. Our findings would be useful for expansion of limited PHHs for use in studies of drug metabolism and toxicity testing.

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Project description:Plasticity of differentiated cells has been proved by nuclear transfer, induced pluripotent cells and transdifferentiation. Here we show that by transduction of 3 factors (FOXA3, HNF1A and HNF4A), human fetal fibroblasts can be converted to hepatocyte-like cells (hiHep cells), expressing hepatic marker genes, and acquiring many mature hepatocyte functions in vitro and in vivo. Human fetal fibroblasts (HFF) were tranfected with 3 liver enriched transcription factors (FOXA3, HNF1A, HNF4A), and converted to hepatocyte-like cells (hiHep cells). HFF and primary human hepatocytes (PHH) serve as control.

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Maintenance of primary hepatocyte functions in vitro by inhibiting mechanical tension-induced YAP activation

Project description:Maintenance of primary hepatocyte functions in vitro by inhibiting mechanical tension-induced YAP activation

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2014-03-06 | GSE42643 | GEO

The extent of liver injury determines hepatocyte fate toward senescence or cancer

Project description:Induction of hepatocyte senescence is known to inhibit hepatocellular carcinoma (HCC). Until now, it has not been clear how the degree of liver injury dictates hepatocyte senescence and carcinogenesis. In this study, we investigated whether the severity of injury determines cell fate decisions between hepatocyte senescence and carcinogenesis. After testing of different degrees of liver injury, we found that hepatocyte senescence is strongly induced in the setting of severe acute liver injury. Longer-term, moderate liver injury did not result into hepatocyte senescence, but instead led to a significant incidence of HCC. In addition, carcinogenesis was significantly reduced by the induction of severe acute injury after chronic moderate liver injury. We conclude that severe acute liver injury leads to hepatocyte senescence along with a low incidence of HCC, whereas chronic moderate injury allows hepatocytes to proliferate rather than to enter into senescence, and correlates with a high incidence of HCC. This study improves our understanding in hepatocyte cell fate decisions and suggests a potential clinical strategy to induce senescence to treat HCC.

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Maintenance of primary hepatocyte functions in vitro by inhibiting mechanical tension-induced YAP activation

Project description:It has been a long-standing challenge to maintain the functions of hepatocytes in vitro. In the present study, we found that mechanical tension-induced yes-associated protein (Yap) activation triggered hepatocyte dedifferentiation. Alleviation of mechanical tension by confinement of cell spreading was sufficient to inhibit hepatocyte dedifferentiation. Based on this finding, we identified a small molecular cocktail LBDXL through reiterative chemical screening that could maintain hepatocyte functions over the long term and in vivo repopulation capacity by targeting actin polymerization and actomyosin contraction.

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Transcriptomic profiling of mutant and WT HNF4alpha hepatic progenitor stage cells

Project description:During mammalian development, liver differentiation is driven by signals which converge on multiple transcription factor networks. The hepatocyte nuclear factor signalling network is known to be essential for hepatocyte specification and maintenance. In these studies we demonstrate that nuclear HNF4a is essential for hepatic progenitor specification and the introduction of point mutations in HNF4a’s SUMO consensus motif leads to disrupted hepatocyte specification and maturation.

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