Plasticity of Hepatic Cell Differentiation: Bipotential Adult Mouse Liver Clonal Cell Lines Competent to Differentiate In Vitro and In Vivo

Fougère-Deschatrette, Catherine; Imaizumi-Scherrer, Tereza; Strick‐Marchand, Hélène; Morosan, Serban; Charneau, Pierre; Kremsdorf, Dina; Faust, Daniela M.; Weiss, Mary C.

doi:10.1634/stemcells.2006-0009

Cited by 69 publications

(54 citation statements)

References 67 publications

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“…Interestingly there was a more than 2-fold increase in the expression of CK-19 during this same time period. These findings are intriguing and we postulate that the sca-HPCs may be dedifferentiating in culture; a similar phenomenon had been demonstrated with mature hepatocytes in culture [25] and with other HPC populations [12]. Using a culture system that supports differentiation of hepatocytic cells along a biliary lineage the sca-HPCs did not differentiate towards a specific phenotype and while there was a loss of AFP expression with persistent expression of CK-19 there was also a decrease in albumin expression.…”

Section: [Data Not Shown]supporting

confidence: 60%

“…Alternative approaches include isolating proliferative populations from the liver using hepatic injury models that inhibit mature hepatocyte replication [8,9]. In addition, bipotent progenitor cells capable of multiple rounds of cell division have been identified without a preceding injury to the liver [10][11][12]. The population of "small hepatocytes" from adult rat liver described by Mitaka et al is mononuclear with a less differentiated morphologic appearance [10].…”

Section: Introductionmentioning

confidence: 99%

“…More recently FougereDeschatrette et al isolated bipotential clonal cell lines from adult murine liver. They demonstrated the persistence of gene transcription of several liver related factors during extended passage along with overlap of select oval cell and biliary markers [12]. In contrast a select human hepatic stem cell population expressed numerous hepatic markers but no hematopoietic or biliary markers [14].…”

Section: Introductionmentioning

confidence: 99%

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Enrichment of a bipotent hepatic progenitor cell from naïve adult liver tissue

Wright

Samuelson

Walkup

et al. 2008

Biochemical and Biophysical Research Communications

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Section: [Data Not Shown]supporting

confidence: 60%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Enrichment of a bipotent hepatic progenitor cell from naïve adult liver tissue

Wright

Samuelson

Walkup

et al. 2008

Biochemical and Biophysical Research Communications

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“…Purified hepatocytes were collected from the bottom of the tube after centrifugation at 1,750 × g for 20 min and were resuspended in DMEM supplemented with 10% (vol/ vol) FCS. Cells were plated at a density of 70 × 10 3 nuclei/cm 2 and were allowed to attach for 1-1.5 h. Then the medium was replaced with William's E medium (Invitrogen) supplemented with 10% FCS, penicillin/streptomycin, 2 mM glutamine, 10 mM nicotinamide, ITS (insulin, transferrin, sodium selenit), 50 ng/mL EGF, and 10 −7 M dexamethasone (48). The typical yield was 40-50 × 10 6 hepatocyte nuclei per mouse liver with 90-93% viability.…”

Section: Methodsmentioning

confidence: 99%

Core circadian protein CLOCK is a positive regulator of NF-κB–mediated transcription

Spengler¹,

Kuropatwinski²,

Comas³

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

271

253

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The circadian clock controls many physiological parameters including immune response to infectious agents, which is mediated by activation of the transcription factor NF-κB. It is widely accepted that circadian regulation is based on periodic changes in gene expression that are triggered by transcriptional activity of the CLOCK/BMAL1 complex. Through the use of a mouse model system we show that daily variations in the intensity of the NF-κB response to a variety of immunomodulators are mediated by core circadian protein CLOCK, which can up-regulate NF-κB-mediated transcription in the absence of BMAL1; moreover, BMAL1 counteracts the CLOCK-dependent increase in the activation of NF-κB-responsive genes. Consistent with its regulatory function, CLOCK is found in protein complexes with the p65 subunit of NF-κB, and its overexpression correlates with an increase in specific phosphorylated and acetylated transcriptionally active forms of p65. In addition, activation of NF-κB in response to immunostimuli in mouse embryonic fibroblasts and primary hepatocytes isolated from Clock-deficient mice is significantly reduced compared with WT cells, whereas Clock-Δ19 mutation, which reduces the transactivation capacity of CLOCK on E-box-containing circadian promoters, has no effect on the ability of CLOCK to up-regulate NF-κB-responsive promoters. These findings establish a molecular link between two essential determinants of the circadian and immune mechanisms, the transcription factors CLOCK and NF-κB, respectively.

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“…Further selection based on c-Met-positivity enriched for H-CFU-C and these cells produced both hepatocytes (albumin-positive) and biliary cells (cytokeratin-19-positive) in culture [57]; EGFP-marked cells from these clonally-derived H-CFU-C also produced hepatocytes and biliary cells when injected into mice and, more surprisingly, were found to apparently differentiate into pancreatic ducts and acini and duodenal mucosal cells when injected directly into these organs. The expression of the α6 integrin, in combination with CK19 and A6 (oval cell marker), also selects for clonogenic cells from adult mice, cells capable of forming hepatocytes and biliary cells in albumin-uPA/SCID mice [58].…”

Section: Mr Alison Et Almentioning

confidence: 99%

Stem cells in liver regeneration, fibrosis and cancer: the good, the bad and the ugly

Alison

Islam

Lim

2008

The Journal of Pathology

199

149

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The worldwide shortage of donor livers to transplant end stage liver disease patients has prompted the search for alternative cell therapies for intractable liver diseases, such as acute liver failure, cirrhosis and hepatocellular carcinoma (HCC). Under normal circumstances the liver undergoes a low rate of hepatocyte 'wear and tear' renewal, but can mount a brisk regenerative response to the acute loss of two-thirds or more of the parenchymal mass. A body of evidence favours placement of a stem cell niche in the periportal regions, although the identity of such stem cells in rodents and man is far from clear. In animal models of liver disease, adopting strategies to provide a selective advantage for transplanted hepatocytes has proved highly effective in repopulating recipient livers, but the poor success of today's hepatocyte transplants can be attributed to the lack of a clinically applicable procedure to force a similar repopulation of the human liver. The activation of bipotential hepatic progenitor cells (HPCs) is clearly vital for survival in many cases of acute liver failure, and the signals that promote such reactions are being elucidated. Bone marrow cells (BMCs) make, at best, a trivial contribution to hepatocyte replacement after damage, but other BMCs contribute to the hepatic collagen-producing cell population, resulting in fibrotic disease; paradoxically, BMC transplantation may help alleviate established fibrotic disease. HCC may have its origins in either hepatocytes or HPCs, and HCCs, like other solid tumours appear to be sustained by a minority population of cancer stem cells.

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Plasticity of Hepatic Cell Differentiation: Bipotential Adult Mouse Liver Clonal Cell Lines Competent to Differentiate In Vitro and In Vivo

Abstract: In fetal liver, bipotential hepatoblasts differentiate into hepatocytes and bile duct cells (cholangiocytes).

Cited by 69 publications

References 67 publications

Enrichment of a bipotent hepatic progenitor cell from naïve adult liver tissue

Enrichment of a bipotent hepatic progenitor cell from naïve adult liver tissue

Core circadian protein CLOCK is a positive regulator of NF-κB–mediated transcription

Stem cells in liver regeneration, fibrosis and cancer: the good, the bad and the ugly

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