Differential expression of fetomodulin and tissue plasminogen activator to characterize parietal endoderm differentiation of F9 embryonal carcinoma cells

Imada, Sumi; Yamaguchi, Harumi; Imada, Masato

doi:10.1016/0012-1606(90)90397-2

Cited by 20 publications

(8 citation statements)

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“…The synergistic action of these two hormones requires a time-dependent change in F9 cells induced by RA. These data are somewhat at variance with those of other investigators who employed receptor activity assays to show that RACT, but not RA alone, induced TM expression (7). We suspect that the relative insensitivity of the biologic activity measurements may have been responsible for the lack of detection of RA-induced TM expression.…”

contrasting

confidence: 56%

“…F9 mouse embryonal carcinoma cells provide a suitable in vitro model to study the developmental regulation ofTM gene expression (7). F9 cells can be either maintained in vitro as undifferentiated stem cells or hormonally induced to differentiate into a restricted number of cell types found within the developing mouse embryo: retinoic acid (RA) converts F9 stem cells to a phenotype that is functionally similar to primitive endoderm (8,9), whereas cultivation of the RAtreated cells in the presence of agents that increase intracellular cAMP causes differentiation to a phenotype resembling extraembryonic parietal endoderm (10).…”

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confidence: 99%

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Thrombomodulin gene regulation by cAMP and retinoic acid in F9 embryonal carcinoma cells.

Weiler-Guettler

Soff

et al. 1992

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

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Thrombomodulin (TM) expression was investigated during differentiation of F9 embryonal carcinoma cells into primitive or parietal endoderm. Exposure of F9 cells to retinoic acid (RA) triggers differentiation into primitive endoderm and induces the appearance of barely detectable amounts of TM mRNA, whereas treatment with dibutyryl cAMP plus theophylline (CT) augments the levels of TM mRNA to a 4-fold greater extent than RA. Exposure of F9 cells to RA plus CT initiates differentiation into parietal endoderm and synergistically increases the levels of TM mRNA by 10-to 12-fold compared with CT. The time-dependent establishment of cooperativity between RA and CT appears to be secondary to RA-induced differentiation to primitive endoderm. The above alterations in TM mRNA levels occur by a transcriptional mechanism as judged by nuclear run-on experiments. Transient gene expression experiments show that the human TM promoter is transactivated by coexpression of the human RA receptor i3. Thus, the mechanism of induction of TM expression in F9 cells undergoing differentiation to parietal endoderm appears to be similar, but not identical, to that noted for other late response genes.

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confidence: 56%

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confidence: 99%

Thrombomodulin gene regulation by cAMP and retinoic acid in F9 embryonal carcinoma cells.

Weiler-Guettler

Soff

et al. 1992

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

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“…This distinction is illustrated in the study by Yoshida et al (43) who showed that iatrogenic toxic renal failure could be distinguished from graft rejection in renal transplantation patients treated with cyclosporine. In EC, TM is mainly up-regulated by cAMP and retinoic acid and down-regulated by endo toxin and inflammatory cytokines (Table 3A) (44)(45)(46)(47)(48)(49)(50)(51)(52)(53)(54)(55). This down-regulation can be poten tiated by interferon g (56) but is antagonized by retinoic acid, IL-4 and IL-13 (57)(58)(59).…”

Section: Tm Metabolism and Regulationmentioning

confidence: 99%

Considering cellular thrombomodulin distribution and its modulating factors can facilitate the use of plasma thrombomodulin as a reliable endothelial marker?

Boffa

1996

Pathophysiol Haemos Thromb

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“…The alternative differentiation pathway to parietal endoderm is induced by treatment of F9 cells with RA and dibutyryl cyclic AMP (dbcAMP) (Strickland et al, 1980). Under these conditions, refractile, highly migratory SSEA-1negative cells are generated (Stricldand et al, 1980;Marotti et al, 1982;Imada et al, 1990) that express elevated levels of collagen IV, laminin, and tissue plasminogen activator (tPA). As in the case of VE, the behavior and biochemical properties of F9-derived PE mimic those properties of PE in the mouse embryo, in which ceils detach from the periphery of the stationary endoderm layer that covers the inner cell mass, migrate along the inner surface of the trophoblast and egg cylinder, and synthesize the proteins characteristic of F9-derived PE.…”

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confidence: 99%

Targeted deletion of beta 1 integrins in F9 embryonal carcinoma cells affects morphological differentiation but not tissue-specific gene expression.

Stephens

Sonne

Fitzgerald

et al. 1993

The Journal of Cell Biology

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Abstract. The integrin superfamily of heterodimeric transmembrane adhesion receptors mediates many cell-cell and cell-matrix interactions whose functions are believed to be critical for normal morphogenesis and differentiation. By eliminating the fll integrin gene through homologous recombination, we have assessed the role of the fll integrin family in the F9 embryonal carcinoma model for endodermal differentiation. F9 cells were unexpectedly found to maintain three copies of the fl 1 gene and complete elimination required three sequential rounds of targeting to generate triple knockout lines (/~1 TKO).Elimination of the/~1 integrin family of adhesion receptors from F9 cells resulted in reduced adhesion to fibronectin, laminin and collagen, but strongly enhanced adhesion to vitronectin. The absence of/31 integrins did not promote significant compensatory upregulation of either t3 or/~5 subunits, both of which are known to act as vitronectin receptors when associated with otv. The loss of fll integrins severely affected morphological differentiation when the/~l-deficient cells were induced to differentiate to either parietal or visceral endoderm. Parietal endoderm derived from ill-deficient cells retained a rounded morphology and migrated poorly on both fibronectin and vitronectin. Visceral endoderm derived from/31-deficient cells were also unable to form a normal, confluent epithelial monolayer; instead, a noncontiguous layer containing clumps of disorganized cells was observed. However, loss of/~1 integrins did not interfere with induction by differentiating agents of tissue-specific gene products for either visceral or parietal endoderm. These results suggest that fll integrins mediate morphological differentiation (migration and epithelial formation) but not tissue-specific gene expression in induced F9 cells, and that these two processes are not necessarily linked in this system. TIt~ proper temporal and spatial differentiation of embryonic cells is a complex process that requires signals initiated by interactions with other cells and with extracellular matrix (ECM). ~ Cells receive information from ECM through cell surface receptors. Of particular importance are the integrins, a family of heterodimeric, transmembrane receptors that interact with both ECM ligands and intracellular components, including cytoskeleton-associated proteins (Darnsky and Werb, 1992;Hynes, 1992). Studies using function-perturbing reagents (e.g., antibodies) have indicated that integrins containing the/31 subunit, in particular, communicate signals that help to regulate the terminal

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Differential expression of fetomodulin and tissue plasminogen activator to characterize parietal endoderm differentiation of F9 embryonal carcinoma cells

Cited by 20 publications

References 14 publications

Thrombomodulin gene regulation by cAMP and retinoic acid in F9 embryonal carcinoma cells.

Thrombomodulin gene regulation by cAMP and retinoic acid in F9 embryonal carcinoma cells.

Considering cellular thrombomodulin distribution and its modulating factors can facilitate the use of plasma thrombomodulin as a reliable endothelial marker?

Targeted deletion of beta 1 integrins in F9 embryonal carcinoma cells affects morphological differentiation but not tissue-specific gene expression.

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