Immunolocalization of extracellular matrix components and integrins during mouse liver development

Shiojiri, Nobuyoshi; Sugiyama, Yoshinori

doi:10.1002/hep.20303

Cited by 77 publications

(77 citation statements)

References 33 publications

(22 reference statements)

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“…22,23 FGF2, HGF, and FGF receptor 1 were only expressed in the spontaneous condition, as shown in Table 3. FGF2 receptor was upregulated in the spontaneous condition as well as the GF condition.…”

Section: Regulation Of Hepatocyte Lineage Commitmentmentioning

confidence: 93%

Embryoid Body–Mediated Differentiation of Mouse Embryonic Stem Cells Along a Hepatocyte Lineage: Insights from Gene Expression Profiles

et al. 2006

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Pluripotent embryonic stem (ES) cells represent a promising renewable cell source for the generation of functional differentiated cells. Previous studies incorporating embryoid body (EB)-mediated stem cell differentiation have, either spontaneously or after growth factor and extracellular matrix protein supplementation, yielded populations of hepatocyte lineage cells expressing mature hepatocyte markers such as albumin (ALB). In an effort to promote ES cell commitment to the hepatocyte lineage, we have evaluated the effects of four culture conditions on albumin and gene expression in differentiating ES cells. Quantitative in situ immunofluorescence and cDNA microarray analyses were used to describe not only lineage specificity but also to provide insights into the effects of disparate culture environments on the mechanisms of differentiation. The results of these studies suggest that spontaneous and collagen-mediated differentiation induce cells with the highest levels of ALB expression but mature liver specific genes were only expressed in the spontaneous condition. Further analysis of gene expression profiles indicated that two distinct mechanisms may govern spontaneous and collagen-mediated differentiation.

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Section: Regulation Of Hepatocyte Lineage Commitmentmentioning

confidence: 93%

Embryoid Body–Mediated Differentiation of Mouse Embryonic Stem Cells Along a Hepatocyte Lineage: Insights from Gene Expression Profiles

et al. 2006

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“…1). 5,21 Studies of Flk1 Ϫ/Ϫ mouse embryos, which lack mature endothelial cells and blood vessels, revealed that although initiation of hepatic development had occurred in these embryos, the liver bud failed to expand, and there was no evidence of hepatoblasts invading the septum transversum mesenchyme. 5 These results suggest not only that the hepatic vasculature develops in concert with the hepatoblasts, but that endothelial cells have an integral role in controlling growth of the hepatic primordium.…”

Section: From Where Do Hepatic Cells Arise?mentioning

confidence: 99%

“…117 In contrast to the parenchyma, the portal mesenchyme is a rich source of extracellular matrix that consists of laminin, nidogen, collagens I and IV, and fibronectin, raising the possibility that the extracellular matrix could influence the fate of hepatoblasts. 21,118,119 Careful immunohistochemical analyses at defined stages of mouse development have revealed that deposition of extracellular matrix components changes quite dramatically during hepatogenesis, which coincides with the onset of biliary epithelial cell differentiation. 21 Consistent with the proposal that extracellular matrix is a significant determinant of hepatoblast cell fate, it has been demonstrated that the profile of gene expression within primary hepatic cultures is significantly affected by the composition of extracellular matrix.…”

Section: What Governs the Establishment Of Hepatic Architecture And Mmentioning

confidence: 99%

“…21,118,119 Careful immunohistochemical analyses at defined stages of mouse development have revealed that deposition of extracellular matrix components changes quite dramatically during hepatogenesis, which coincides with the onset of biliary epithelial cell differentiation. 21 Consistent with the proposal that extracellular matrix is a significant determinant of hepatoblast cell fate, it has been demonstrated that the profile of gene expression within primary hepatic cultures is significantly affected by the composition of extracellular matrix. 79,80,118,[120][121][122][123] For example, culture of bipotential mouse embryonic liver cells in matrigel, a soluble basement membrane preparation that includes laminin, collagen IV, heparan sulfate proteoglycans, and entactin, induced them to express biliary epithelial cell markers and form ductile like structures.…”

Section: What Governs the Establishment Of Hepatic Architecture And Mmentioning

confidence: 99%

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Embryonic development of the liver

2005

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“…Given that α6 is expressed in embryonic endothelium from around E13.5 onwards [42][43][44], the fact that the α6fl/fl-Tie1Cre+ mice are born at normal Mendelian ratios suggests that the embryos either lack or overcome any gross angiogenic defect. Our data showing enhanced angiogenesis after endothelial α6-integrin deletion is somewhat reminiscent of the effect of β3-integrin deletion in mice, where global deletion of β3-integrins enhances tumour growth, tumour angiogenesis, and endothelial VEGFR2 levels [30,33,45].…”

Section: Discussionmentioning

confidence: 99%

Genetic ablation of the alpha 6‐integrin subunit in Tie1Cre mice enhances tumour angiogenesis

Germain

Arcangelis

Robinson

et al. 2009

The Journal of Pathology

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Laminins are expressed highly in blood vessel basement membranes and have been implicated in angiogenesis. α6β1-and α6β4-integrins are major receptors for laminins in endothelial cells, but the precise role of endothelial α6-integrin in tumour angiogenesis is not clear. We show that blood vessels in human invasive ductal carcinoma of the breast have decreased expression of the α6-integrin-subunit when compared with normal breast tissue. These data suggest that a decrease in α6-integrin-subunit expression in endothelial cells is associated with tumour angiogenesis. To test whether the loss of the endothelial α6-integrin subunit affects tumour growth and angiogenesis, we generated α6fl/fl-Tie1Cre+ mice and showed that endothelial deletion of α6-integrin is sufficient to enhance tumour size and tumour angiogenesis in both murine B16F0 melanoma and Lewis cell lung carcinoma. Mechanistically, endothelial α6-integrin deficiency elevated significantly VEGF-mediated angiogenesis both in vivo and ex vivo. In particular, α6-integrin-deficient endothelial cells displayed increased levels of VEGF-receptor 2 (VEGFR2) and VEGF-mediated downstream ERK1/2 activation. By developing the first endothelial-specific α6-knockout mice, we show that the expression of the α6-integrin subunit in endothelial cells acts as a negative regulator of angiogenesis both in vivo and ex vivo.

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Immunolocalization of extracellular matrix components and integrins during mouse liver development

Cited by 77 publications

References 33 publications

Embryoid Body–Mediated Differentiation of Mouse Embryonic Stem Cells Along a Hepatocyte Lineage: Insights from Gene Expression Profiles

Embryoid Body–Mediated Differentiation of Mouse Embryonic Stem Cells Along a Hepatocyte Lineage: Insights from Gene Expression Profiles

Embryonic development of the liver

Genetic ablation of the alpha 6‐integrin subunit in Tie1Cre mice enhances tumour angiogenesis

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