Expression of the cytokeratin endo A gene during early mouse embryogenesis.

Duprey, Philippe; Morello, Dominique; Vasseur, Marc; Babinet, Charles; Condamine, Hubert; Brûlet, Philippe; Jacob, François

doi:10.1073/pnas.82.24.8535

Cited by 91 publications

(45 citation statements)

References 19 publications

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“…To determine whether these cells belong to the lineages of either the primitive endoderm, the VE or the PE, we examined the expression of HNF4 and Troma1 in the Mp -/-EBs. Troma1 (Duprey et al, 1985;Verheijen et al, 1999), a marker for PrE, did not stain any of the Mp -/-EB cells. However, HNF4 was present in most of the Mp -/-EB cells.…”

Section: Discussionmentioning

confidence: 99%

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Maspin plays an essential role in early embryonic development

et al. 2004

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Maspin (Mp) is a member of the serpin family with inhibitory functions against cell migration, metastasis and angiogenesis. To identify its role in embryonic development in vivo, we generated maspin knockout mice by gene targeting. In this study, we showed that homozygous loss of maspin expression was lethal at the peri-implantation stage. Maspin was specifically expressed in the visceral endoderm after implantation; deletion of maspin interfered with the formation of the endodermal cell layer, thereby disrupting the morphogenesis of the epiblast. In vitro, the ICM of the Mp–/– blastocysts failed to grow out appropriately. Data from embryoid body formation studies indicated that the Mp–/– EBs had a disorganized, endodermal cell mass and lacked a basement membrane layer. We showed that the embryonic ectoderm lineage was lost in the Mp–/– EBs,compared with that of the Mp+/+ EBs. Re-expression of maspin partially rescued the defects observed in the Mp–/– EBs, as evidenced by the appearance of ectoderm cells and a layer of endoderm cells surrounding the ectoderm. In addition, a maspin antibody specifically blocked normal EB formation,indicating that maspin controls the process through a cell surface event. Furthermore, we showed that maspin directly increased endodermal cell adhesion to laminin matrix but not to fibronectin. Mp+/–endodermal cells grew significantly slower than Mp+/+endodermal cells on laminin substrate. We conclude that deletion of maspin affects VE function by reducing cell proliferation and adhesion, thereby controlling early embryonic development.

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Section: Discussionmentioning

confidence: 99%

“…4D). We further stained the EBs with an antibody against Troma1, a marker for the PrE lineage (Duprey et al, 1985;Verheijen et al, 1999). Not a single cell in either the Mp +/+ or the Mp -/-EBs stained positively for Troma1 (data not shown).…”

Section: Mp -/-Embryoid Bodies Exhibit a Disorganized Layer Of Viscermentioning

confidence: 99%

Maspin plays an essential role in early embryonic development

et al. 2004

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“…EndoA/K8/TROMA-1 is expressed in all early endoderm cells (Duprey et al, 1985), whereas THBD, encoding thrombomodulin, is highly expressed specifically in PE and has been used as a cell type marker for PE in EBs (Thompson and Gudas, 2002;Weiler-Guettler et al, 1992). In day 13 EBs, EndoA is highly expressed and is present in the majority of EBs.…”

Section: Tgf␤1 Reduces Hematopoiesis In Ebsmentioning

confidence: 99%

TGFβ inhibition of yolk-sac-like differentiation of human embryonic stem-cell-derived embryoid bodies illustrates differences between early mouse and human development

Poon

Clermont

Firpo

et al. 2006

Journal of Cell Science

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Transforming growth factor β (TGFβ) plays an important role in development and maintenance of murine yolk sac vascular development. Targeted deletions of Tgfb1 and other components of this signaling pathway, such as Acvrl1, Tgfbr1 and Tgfbr2, result in abnormal vascular development especially of the yolk sac, leading to embryonic lethality. There are significant differences between murine and primate development that limit interpretation of studies from mouse models. Thus, to examine the role of TGFβ in early human vascular development we used the model of differentiating human embryonic stem cell-derived embryoid bodies to recapitulate early stages of embryonic development. TGFβ was applied for different time frames after initiation of embryoid body cultures to assess its effect on differentiation. TGFβ inhibited the expression of endodermal, endothelial and hematopoietic markers, which contrasts with findings in the mouse in which TGFβ reduced the level of endodermal markers but increased endothelial marker expression. The inhibition observed was not due to changes in proliferation or apoptosis. This marked contrast between the two species may reflect the different origins of the yolk sac hemangiogenic lineages in mouse and human. TGFβ effects on the hypoblast, from which these cell lineages are derived in human, would decrease subsequent differentiation of hematopoietic, endothelial and endodermal cells. By contrast, TGFβ action on murine hypoblast, while affecting endoderm would not affect the hemangiogenic lineages that are epiblast-derived in the mouse. This study highlights important differences between early human and mouse embryonic development and suggests a role of TGFβ in human hypoblast differentiation.

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“…(Hogan et al 1983;Silver et al 1983). Whereas undifferentiated murine EC cells do not express mouse K18 or K8, spontaneous or retinoic-acid-induced differentiation results in increased transcription of the respective genes , appearance of the mRNAs and proteins, and their assembly into immunologically detectable IFs (Oshima 1981(Oshima , 1982Tabor and Oshima 1982;Duprey et al 1985). Although neither EC cells nor most differentiated, nonepithelial cells such as fibroblasts express K18, the reasons that the two cell types do not express endogenous K18 appear to differ.…”

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confidence: 99%

“…Among the earliest differentially expressed genes are members of the intermediate filament (IF) gene family, the keratins (Steinert and Parry 1985). Endo B, the mouse form of human keratin 18 (K18), is a type I keratin protein that is first expressed just prior to blastocyst formation along with its normally coexpressed and complementary type II keratin partner, Endo A (Brfilet et al 1980;Oshima et al 1983;Duprey et al 1985). Expression of both proteins is restricted at the blastocyst stage to the trophectoderm and extraembryonic endoderm (Brfilet et al 1980;Jackson et al 1980;Chisholm and Houliston 1987).…”

mentioning

confidence: 99%