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PubMed2000

The H19 endodermal enhancer is required for Igf2 activation and tumor formation in experimental liver carcinogenesis.

The expression of the linked but reciprocally imprinted Igf2 and H19 genes is activated in adult liver in the course of tumor development. By in situ hybridization analysis we have shown that both the Igf2 and H19 RNAs are expressed in the majority of the neoplastic nodules, and that hepatocellular carcinomas are developed in an experimental model of liver carcinogenesis. H19 is also highly activated in smaller and less distinct hyperplastic regions. The few neoplastic areas showing Igf2 but no H19 RNA display loss of the maternally inherited allele at the Igf2/H19 locus. These data are compatible with the existence of a common activation mechanism of these two genes during liver carcinogenesis and with a stronger H19 induction in the pre-neoplastic lesions. By using mice carrying a deletion of the H19 endodermal enhancer, we show that this regulatory element is necessary for the activation of the Igf2 and H19 genes upon induction of liver carcinogenesis. Furthermore, multiple sites of the H19 endodermal enhancer region become hypersensitive to DNase I when the carcinogenesis process is induced. Lastly, liver tumors developed in mice paternally inheriting the H19 enhancer deletion are found to have marked growth delays, increased frequency of apoptotic nuclei, and lack of Igf2 mRNA expression, thus indicating that this regulatory element plays a major role in the progression of liver carcinogenesis, since it is required for the activation of the anti-apoptotic Igf2 gene.

Animals↗
PubMed2003

Neurogenin3 triggers beta-cell differentiation of retinoic acid-derived endoderm cells.

Neurogenin3 is a member of the basic helix-loop-helix ('bHLH') family of transcription factors. It plays a crucial role in the commitment of embryonic endoderm into the pancreatic differentiation programme. This factor is considered to act upstream of a cascade of other transcription factors, leading to the fully differentiated endocrine phenotype. Direct observation of the sequential activation of these factors starting from Neurogenin3 had never been demonstrated. By using retinoic acid-derived-endoderm F9 cells as a model, the present study indicates that the ectopic expression of Neurogenin3 is able to start the differentiation pathway of endocrine pancreas. Neurogenin3 triggers the expression of several pancreatic transcription factors following a well defined temporal activation sequence. By reverse transcriptase PCR, immunohistochemistry and RIA, it is shown that stable transfected cells are able to form embryod bodies that produce insulin in response to glucose stimulation. This is the first report of a differentiation event induced by the ectopic expression of a transcription factor in embryonic pluripotent stem cells.

Animals↗
PubMed2002

In the multiheaded strain (mh-1) of Hydra magnipapillata the ectodermal epithelial cells are responsible for the formation of additional heads and the endodermal epithelial cells for the reduced ability to regenerate a foot.

Hydra consist of three self-renewing cell lineages: the ectodermal epithelial, endodermal epithelial and interstitial cell lineages. The role of these cell lineages in head formation and foot regeneration in Hydra magnipapillata was studied by comparing the multiheaded strain mh-1 with the wild-type. Adult polyps of this strain show a reduced ability to regenerate a foot in the apical body half several days before additional heads are formed there. Cell lineage chimeras were produced, and it was found that in mh-1, the ectodermal epithelial cell lineage is responsible for the formation of additional heads, whereas the endodermal epithelial cell lineage and, to a lesser extent, the derivatives of the interstitial cell lineage, are responsible for the reduced ability of foot regeneration.

Animals↗
PubMed2003

Signals from primary mesenchyme cells regulate endoderm differentiation in the sea urchin embryo.

Primary mesenchyme cells (PMC), the skeletogenic cells derived from the micromeres of the sea urchin embryo, are involved in the differentiation of the gut. When PMC were deleted from the mesenchyme blastula, both formation of the constrictions in the gut and expression of endoderm-specific alkaline phosphatase were significantly delayed. Therefore, the correct timing of gut differentiation depends on the existence of PMC, probably via a type of promotive signal. To date, the only role of PMC in other tissue differentiation has been a suppressive signal for the conversion of secondary mesenchyme cells (SMC) into skeletogenic cells. The present experiments using PMC ablation and transplantation showed that both signaling processes occurred in the same short period during gastrulation, but the embryos kept their competence for gut differentiation until a later stage. Further investigations indicated that conversion of SMC did not cause delay in gut differentiation and that SMC did not mediate the PMC signal to the endoderm. Therefore, the effect of PMC on gut differentiation could be a new role that is independent of the suppressive effect for SMC conversion.

Alkaline Phosphatase↗
PubMed2002

Embryonic macrophages of early rat yolk sac: Immunohistochemistry and ultrastructure with reference to endodermal cell layer.

Macrophages are multifunctional cells that participate in numerous biological processes; they actively phagocytose foreign particles and cell debris. Embryonic tissue macrophages are present at early stages of mammalian development; their ontogeny and function is still under investigation. Our study used immunohistochemistry and electron microscopy to investigate early rat yolk sac macrophages using mouse antirat macrophage monoclonal antibodies (mAb) Mar 1 and Mar 3 produced by our laboratory. Mar 3 mAb revealed the first emergence of immature macrophages in the rat yolk sac at fetal day nine coinciding with the beginning of yolk sac haemopoiesis that consisted mainly of erythropoiesis, while Mar 1 mAb detected specifically rat yolk sac macrophages at about the 13th to 14th day of gestation. Immunoreactivity against Mar mAbs was mainly located in the yolk sac endodermal cell layer, which may signify endodermal origin of the yolk sac macrophages. Ultrastructurally mature yolk sac macrophages contained numerous endocytic vesicles or vacuoles, well-developed Golgi saccules and many electron dense granules in their cytoplasm and a number of microvillous projections from the cell surface. After establishment of the circulation between yolk sac and embryo, Mar 3 positive cells were also demonstrated inside fetal undifferentiated mesenchymal tissue at fetal day 12. The study demonstrated the first emergence of immature yolk sac macrophages being among the earliest haemopoietic cells formed in mammalian development. Thus, Mar mAbs managed to detect macrophage differentiation antigens through their development early in the rat yolk sac.

Animals↗
PubMed2002

Primary endodermal sinus (yolk sac) tumour of the liver.

Primary endodermal sinus tumour of the liver is an extremely rare neoplasm. A 37-year-old man presented with a mass in the left lobe of the liver and a raised serum alpha-fetoprotein concentration. A left hepatic lobectomy was performed. Histological examination revealed an endodermal sinus tumour of the liver. There was no evidence of an extrahepatic primary source.

Adult↗
PubMed2005

Endodermal cyst anterior and anterolateral to the brainstem: a report of an experience with seven cases.

We report our experience with seven cases of endodermal cysts located anterior and anterolateral to the brainstem. The ages of the patients ranged from 10 to 35 years. There were three males and four females. The cysts had characteristic imaging features, and contained fluid having a 'greenish-yellow pus-like' hue and consistency varied from thin watery fluid to colloid gel like material. The capsule of the tumour was relatively thin. A radical resection of the cyst contents was done in all cases. Because of the thin nature of capsule, wide extensions and intimate relationship with critical nerves and vessels, complete resection of the cyst wall was possible only in one case, whilst in others the wall was partially resected. All patients showed a rapid symptomatic and neurological recovery. During the average follow-up period of 53 months, there has been no recurrence in the cyst and all patients are leading normal lives. In this presentation, the clinical and radiological features and surgical management of endodermal cysts are discussed and the relevant literature is briefly reviewed. It appears that evacuation of the cyst contents and partial resection of the cyst wall could be a safe treatment option in these cases.

Adolescent↗
PubMed1999

Absence of basement membranes after targeting the LAMC1 gene results in embryonic lethality due to failure of endoderm differentiation.

The LAMC1 gene coding for the laminin gamma1 subunit was targeted by homologous recombination in mouse embryonic stem cells. Mice heterozygous for the mutation had a normal phenotype and were fertile, whereas homozygous mutant embryos did not survive beyond day 5.5 post coitum. These embryos lacked basement membranes and although the blastocysts had expanded, primitive endoderm cells remained in the inner cell mass, and the parietal yolk sac did not develop. Cultured embryonic stem cells appeared normal after targeting both LAMC1 genes, but the embryoid bodies derived from them also lacked basement membranes, having disorganized extracellular deposits of the basement membrane proteins collagen IV and perlecan, and the cells failed to differentiate into stable myotubes. Secretion of the linking protein nidogen and a truncated laminin alpha1 subunit did occur, but these were not deposited in the extracellular matrix. These results show that the laminin gamma1 subunit is necessary for laminin assembly and that laminin is in turn essential for the organization of other basement membrane components in vivo and in vitro. Surprisingly, basement membranes are not necessary for the formation of the first epithelium to develop during embryogenesis, but first become required for extra embryonic endoderm differentiation.

Animals↗
PubMed2004

Regulation of Ras-MAPK pathway mitogenic activity by restricting nuclear entry of activated MAPK in endoderm differentiation of embryonic carcinoma and stem cells.

In response to retinoic acid, embryonic stem and carcinoma cells undergo differentiation to embryonic primitive endoderm cells, accompanied by a reduction in cell proliferation. Differentiation does not reduce the activation of cellular MAPK/Erk, but does uncouple mitogen-activated protein kinase (MAPK) activation from phosphorylation/activation of Elk-1 and results in inhibition of c-Fos expression, whereas phosphorylation of the cytoplasmic substrate p90RSK remains unaltered. Cell fractionation and confocal immunofluorescence microscopy demonstrated that activated MAPK is restricted to the cytoplasmic compartment after differentiation. An intact actin and microtubule cytoskeleton appears to be required for the restriction of MAPK nuclear entry induced by retinoic acid treatment because the cytoskeletal disrupting agents nocodazole, colchicine, and cytochalasin D are able to revert the suppression of c-Fos expression. Thus, suppression of cell proliferation after retinoic acid-induced endoderm differentiation of embryonic stem and carcinoma cells is achieved by restricting nuclear entry of activated MAPK, and an intact cytoskeleton is required for the restraint.

Active Transport, Cell Nucleus↗
PubMed2005

Overexpression of Nodal promotes differentiation of mouse embryonic stem cells into mesoderm and endoderm at the expense of neuroectoderm formation.

Understanding how to direct the fate of embryonic stem (ES) cells upon differentiation is critical to their eventual use in therapeutic applications. Clues for controlling ES cell differentiation may be found in the early embryo because mouse ES cells form derivatives of all three embryonic germ layers upon injection into blastocysts. One promising candidate for influencing the differentiation of ES cells into the embryonic germ layers is the transforming growth factor-beta (TGF-beta) growth factor, Nodal. Nodal null mouse mutants lack mesoderm, and injection of Nodal mRNA into nonmammalian embryos induces mesodermal and endodermal tissues. We find that overexpression of Nodal in mouse ES cells leads not only to up-regulation of mesodermal and endodermal cell markers but also to downregulation of neuroectodermal markers. These findings demonstrate the importance of Nodal's influence on the differentiation of pluripotent cells to all three of the primary germ layers. Accordingly, altering expression of factors responsible for cell differentiation in the intact embryo provides an approach for directing ES cell fates in vitro toward therapeutically useful cell types.

Animals↗
PubMed1994

The endodermal sinus tumour and clear cell ovarian cancer.

There are similarities between clear cell epithelial ovarian carcinoma and endodermal sinus tumours. Apart from the morphological and clinical characteristics there are immunohistochemical markers of value in differentiating these 2 tumours and the detection of a raised serum AFP is characteristic of endodermal sinus tumours. These 3 cases we describe show the fallibility of the classical differentiating criteria between these two tumours.

Adenocarcinoma, Clear Cell↗
PubMed1986

Isolation and characterization of the cDNAs corresponding to mRNAs abundant in undifferentiated mouse embryonal teratocarcinoma stem cells, but not in differentiated mouse parietal endoderm cells.

As retinoic acid (RA) and dibutyryl cAMP (cAMP) treatment induces differentiation of mouse teratocarcinoma F9 cells into parietal endoderm cells in vitro, we initiated studies on the molecular mechanisms underlying early mammalian cell differentiation in this system. We constructed cDNA libraries on the poly(A)+RNAs extracted from the undifferentiated F9 cells, and screened for cDNA sequences expressed abundantly in F9 cells, but not in terminally differentiated mouse parietal endoderm PYS-2 cells. Six different cDNA clones were isolated and characterized. The levels of RNAs hybridizable to these clones were at most 5 to 24% in the PYS-2 cells when compared with those in the undifferentiated F9 cells. The six clones were classified into two groups on the basis of their responses to the RA and cAMP treatment. In F9 cells, the levels of RNAs hybridizable to the first group, which contained four clones, were decreased within 72 h after the addition of RA and cAMP, while those of the second group, which contained the remaining two clones, did not decrease significantly. One of the first group clones, named pF9-1, corresponded to the mouse "early transposon-like elements" and another, named pF9-4, hybridized to multi-size RNAs extracted from the undifferentiated F9 cells. The mouse genomic DNA sequences hybridizable to pF9-4 were repeated approximately 5,000 times, and comprise a new gene family, the expression of which is developmentally regulated in mouse F9 cells.

Animals↗
PubMed1994

Disruption of the HNF-4 gene, expressed in visceral endoderm, leads to cell death in embryonic ectoderm and impaired gastrulation of mouse embryos.

Expression of HNF-4, a transcription factor in the steroid hormone receptor superfamily, is detected only in the visceral endoderm of mouse embryos during gastrulation and is expressed in certain embryonic tissues from 8.5 days of gestation. To examine the role of HNF-4 during embryonic development, we disrupted the gene in embryonic stem cells and found that the homozygous loss of functional HNF-4 protein was an embryonic lethal. Cell death was evident in the embryonic ectoderm at 6.5 days when these cells normally initiate gastrulation. As assessed by expression of Brachyury and HNF-3 beta, primitive streak formation and initial differentiation of mesoderm do occur, but with a delay of approximately 24 h. Development of embryonic structures is severely impaired. These results demonstrate that the expression of HNF-4 in the visceral endoderm is essential for embryonic ectoderm survival and normal gastrulation.

Animals↗
PubMed1982

Mechanisms of adhesion among cells of the early chick blastoderm: role of the beta-D-galactoside-binding lectin in the adhesion of extraembryonic endoderm cells.

Cells from the extraembryonic endoderm of the gastrulating chick embryo contain a beta-D-galactoside-binding lectin inhibited by thiodigalactoside (TDG). TDG inhibits the aggregation of freshly prepared cells. In these fresh cell suspensions, adhesion is also inhibited when purified lectin is added to the aggregation assay. If these cells are incubated at 22 degrees C their adhesion decreases. Associated with this is an increase in lectin activity in the cell supernatants. In these incubated cells aggregation is stimulated by TDG and desialyzed fetuin. These data suggest that the lectin may have a role to play in cellular adhesion. Under some experimental conditions extraembryonic endoderm cells from rosettes with trypsinized glutaraldehyde-fixed rabbit erythrocytes. This phenomenon is inhibited, to a certain extent, by TDG.

Animals↗
PubMed1985

Distinct properties of receptors for Dolichos biflorus agglutinin (DBA) isolated from small intestine of adult mice and endoderm cells of early embryos and teratocarcinomas.

Receptors for Dolichos biflorus agglutinin are only expressed in severely restricted cell populations of the mouse. The receptors were isolated from mouse embryos, teratocarcinoma cells, and the small intestine of adult mice. Upon SDS-polyacrylamide gel electrophoresis, all of the receptor preparations migrated as distinct glycoprotein bands; the apparent molecular weights were more than 150 kilodaltons in all cases. The sizes of the carbohydrate moieties determined by gel filtration after alkaline NaBH4 treatment appeared to correlate with the status of cell differentiation. Thus, as has previously been reported, the receptors from teratocarcinoma OTT6050 and embryonal carcinoma cells (F9 and N4-1) contained large amounts of high-molecular-weight carbohydrates eluted near the excluded volume of a Sephadex-G-50 column. The receptors from 6.5-day embryos also contained high-molecular-weight carbohydrates, whose average molecular weight was lower than those obtained from OTT6050, F9, or N4-1. The receptors from PYS-2 parietal endoderm cells, END-C-2 visceral endoderm cells, and the small intestine did not contain significant amounts of the large carbohydrates. These results illustrate the complex nature of the cell-surface changes accompanying cell differentiation.

Animals↗
PubMed1992

Disruption of the cytoskeleton-extracellular matrix linkage promotes the accumulation of plasminogen activators in F9 derived parietal endoderm.

When F9 teratocarcinoma cells are treated with retinoic acid plus cyclic AMP (RACF9) they differentiate into parietal endoderm. Differentiation is accompanied by the acquisition of substrate adhesion sites and a change in the pattern of gene expression, including the synthesis of tissue-type plasminogen activator (tPA). We demonstrate here that dihydrocytochalasin B (DHCB) treatment of differentiating F9 cells prevents the assembly of a structured actin cytoskeleton and generates a more rounded and stellate cell morphology. This morphological change is accompanied by the accumulation of the usually visceral endoderm-specific marker urokinase-type plasminogen activator (uPA) and an increase in tPA levels in comparison to untreated RACF9 controls. The increase in tPA accumulation is preceded by an increase in tPA mRNA levels. These effects are reversible, with a lag, when DHCB is removed, and PA accumulation can be stimulated within 24 h when differentiated cells are exposed to DHCB. Exposure to the microtubule disrupting agent colchicine has no effect on uPA or tPA accumulation. In addition, antibody directed against the beta 1 integrin subunit can also specifically elicit increased PA production. Thus disturbing the cytoskeleton and cytoskeleton associated substrate adhesions promotes PA accumulation.

Actins↗
PubMed1994

Sudden death due to pulmonary tumor embolism in a patient with endodermal sinus tumor of the ovary.

Only 2 cases of fatal pulmonary tumor embolism have been described in patients having malignant tumors of the ovary. Both were diffuse microtumor emboli in the pulmonary arteries of elderly individuals. We present a teen-aged patient who died suddenly due to a massive tumor embolism of the right main pulmonary artery after a two-year remission of an endodermal sinus tumor of the ovary. Upon her first admission, she was treated with radical operation and insufficient chemotherapy. Two years later, she was readmitted to our hospital because of the sudden onset of dyspnea and shock; and she died 5 hours after readmission. A case of endodermal sinus tumor of the ovary with fatal pulmonary tumor embolism is described.

Adolescent↗
PubMedDate not supplied

Disseminated peritoneal tuberculosis mimicking advanced-stage endodermal sinus tumor: a case report.

It is well known that peritoneal tuberculosis may mimic advanced-stage epithelial ovarian carcinoma because of similar clinical, radiologic, and laboratory findings. However, disseminated peritoneal tuberculosis mimicking advanced-stage endodermal sinus tumor (ESS) has not been reported previously. An 18-year-old nulliparous woman came with the complaint of pelvic pain and weight loss. Imaging studies demonstrated that she had multiple peritoneal implants and left adnexial mass. Also, laboratory studies showed elevated CA125 and alpha fetoprotein levels suggesting an initial diagnosis of ESS. However, intraoperative frozen section examination showed caseous necrosis, and she was diagnosed as having disseminated peritoneal tuberculosis. Two months after the initial exploration, the patient required liver transplantation because of hepatic failure due to widespread hepatic involvement of the tuberculosis. Concomitant peritoneal and hepatic involvement of tuberculosis may cause false elevation of multiple tumor markers of gynecological cancers and may lead to misdiagnosis and mismanagement of patients. Elevation of these markers should be carefully investigated especially in premenopausal women. To our knowledge, this is the first reported case of peritoneal tuberculosis misdiagnosed as endodermal sinus tumor.

Adolescent↗