Effects of growth and differentiation factors on the epithelial-mesenchymal transition in cultured neonatal rat hepatocytes

Pagan, Roser; Sánchez, Aránzazu; Martín, Isabel Fernández de Castro; Llobera, Miquel; Fabregat, Isabel; Vilaró, Senén

doi:10.1016/s0168-8278(99)80292-x

Cited by 41 publications

(31 citation statements)

References 38 publications

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“…OSM may act in concert with glucocorticoids (contained in the culture medium), other cytokines such as transforming growth factor-␤, epidermal growth factor, and hepatocyte growth factor, and adhesion molecules such as fibronectin. [53][54][55] We also confirmed that hepatocytic maturation of fetal liver stroma parallels the decline in hematopoietic supporting ability. OSM decreased, by 4-fold, week 5 CAFCs generated in the presence of AFT024 cells while inducing a clear-cut shift from an EMT to a hepatocytic phenotype in cells from this line.…”

Section: Discussionsupporting

confidence: 72%

Fetal liver stroma consists of cells in epithelial-to-mesenchymal transition

Chagraoui

Lepage-Noll

Anjo

et al. 2003

Blood

141

100

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Liver becomes the predominant site of hematopoiesis by 11.5 dpc (days after coitus) in the mouse and 15 gestational weeks in humans and stays so until the end of gestation. The reason the liver is the major hematopoietic site during fetal life is not clear. In this work, we tried to define which of the fetal liver microenvironmental cell populations would be associated with the development of hematopoiesis and found that a population of cells with mixed endodermal and mesodermal features corresponded to hematopoieticsupportive fetal liver stroma. Stromal cells generated from primary cultures or stro-

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Section: Discussionsupporting

confidence: 72%

Fetal liver stroma consists of cells in epithelial-to-mesenchymal transition

Chagraoui

Lepage-Noll

Anjo

et al. 2003

Blood

141

100

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“…Nevertheless, in our study, TGF-β1 has been shown to promote apoptosis in FAO cells, as was shown elsewhere in normal hepatocytes. Although this cytokine inhibits growth and promotes programmed cell death, it might also induce differentiation in fetal hepatocytes in the presence of survival signals, such as EGF [36][37][38]. To some extent this confirms the similar effect on CNT2 expression triggered by glucocorticoids, shown elsewhere in rat fetal hepatocytes (along with thyroid hormone) [11] and, recently, in a rat enterocyte cell model, IEC6 [39].…”

Section: Discussionsupporting

confidence: 78%

TGF-β transcriptionally activates the gene encoding the high-affinity adenosine transporter CNT2 in rat liver parenchymal cells

Valdés

Fernández‐Veledo

Aymerich

et al. 2006

Cell. Mol. Life Sci.

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The nucleoside transporter CNT2 is the highest-affinity adenosine transporter identified so far. Recent evidence suggests that CNT2 has functions other than salvage (i.e. modulation of purinergic responses). Here we identified TGF-beta1 as a potent inducer of CNT2 protein expression in liver parenchymal cells. By contrast, CNT1, which is a target of multifunctional cytokines involved in liver cell proliferation, does not respond to TGF-beta1 treatment. Cloning of a murine CNT2 gene sequence with promoter-like activity enabled us to demonstrate that this cytokine exerts this effect by transcriptionally activating the CNT2-encoding gene in a JNK-dependent manner. The evidence that CNT2 is not a target of multifunctional cytokines involved in hepatocyte proliferation, but instead, of a cytokine that plays major roles in differentiation and apoptosis, further supports the view that the main physiological role of this transporter protein is not nucleoside salvage.

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“…Indeed, in vitro studies have shown that cultured neonatal rat hepatocytes are capable of undergoing EMT at certain conditions. 43,44 The process of hepatocyte EMT involves the loss of their typical differentiation markers, the acquisition of a migrating morphology, and a change in the expression of the intermediate filament protein cytokeratin to vimentin. [43][44][45] Although BECs can transform to myofibroblasts and apparently migrate into the periductal region via the impaired basement membrane, it is conceivable that the periductal myofibroblasts may originate from other sources as well.…”

Section: Discussionmentioning

confidence: 99%

“…43,44 The process of hepatocyte EMT involves the loss of their typical differentiation markers, the acquisition of a migrating morphology, and a change in the expression of the intermediate filament protein cytokeratin to vimentin. [43][44][45] Although BECs can transform to myofibroblasts and apparently migrate into the periductal region via the impaired basement membrane, it is conceivable that the periductal myofibroblasts may originate from other sources as well. 35,36 We envision that hepatic stellate cells, residential fibroblasts, BECs, and perhaps bone marrow-derived cells, all contribute to the periductal myofibroblast pool after BDL.…”

Section: Discussionmentioning

confidence: 99%