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PubMed2001

Spinal intradural endodermal cyst located anterior to the cervical spinal cord.

Spinal endodermic cysts are rare and may be associated with other congenital anomalies (mediastinal cysts, bony defects of the vertebral body), derive from defective displacement of the endoderm of the intestinal tract or, more rarely, the respiratory one. The authors describe a case of endodermic cyst of the cervical spine localized anteriorly to the spinal cord. In the case we treated the patient was a 17-year-old male who presented hypostenia of the lower limbs accompanied by hyperreflexia and spasticity; physical examination was negative. MRI, CT and CT-myelography documented a well-defined mass situated anteriorly to the spinal cord at C2-C4 level. A total-body CT-scan excluded the existence of other malformations. Surgery was performed via an anterior approach and the cyst completely removed. Histological examination confirmed the endodermal nature of the cyst. At long-term follow-up examination the patient was neurologically intact. Postoperative MRI showed a small residue of the cyst wall without spinal cord compression. Endodermic spinal cysts are very rare intradural lesions, predominantly with an anterior cervical localization, which derive from misplaced embryonic and endodermic cells. In the majority of cases, clinical onset is insidious and has a discontinuous progression. The best diagnostic tool is MRI. Treatment of choice is total surgical removal or emptying of the cyst followed by fenestration.

Adolescent↗
PubMed1998

Maternal and zygotic expression of the endoderm-specific alkaline phosphatase gene in embryos of the ascidian, Halocynthia roretzi.

Alkaline phosphatase (AP) activity is expressed by endodermal cells of ascidian larvae. It was reported previously that the expression of AP activity is resistant to treatment with actinomycin D, a transcription inhibitor that inhibits the appearance of several other tissue-specific molecules and morphological markers of tissue formation in developing ascidians. The resistance of AP expression to actinomycin D treatment suggests that endodermal AP activity does not depend on zygotic transcription and that its appearance is mediated by the translational activation of maternal AP mRNA present in ascidian eggs. However, it was also shown that anucleate merogons do not develop AP activity. To directly examine whether maternal AP transcripts are present in the cytoplasm of eggs, we isolated a cDNA of an endoderm-specific AP in Halocynthia roretzi and examined the temporal and spatial expressions of this gene during embryogenesis using Northern blots and in situ hybridization. Maternal AP transcripts were detected in oocytes, cleaving-stage embryos, and in gastrulae, and endoderm-specific AP transcripts dramatically increased about 14 times from the neurula stage to the larval stage in endoderm precursor cells. These results suggest that the differentiation of endoderm is primarily correlated with the activation of zygotic transcription of the AP gene, presumably by egg cytoplasmic factors, similar to how muscle and epidermis are believed to develop.

Alkaline Phosphatase↗
PubMed1994

Hepatocytic transcription factor expression in human embryonal carcinoma and yolk sac carcinoma cell lines: expression of HNF-3 alpha in models of early endodermal cell differentiation.

Retinoic acid treatment of the multipotent human embryonal carcinoma cell line GCT 27 X-1 induced differentiation into an epithelial cell type which morphologically resembled rodent visceral endoderm in vitro. The differentiated cells expressed some markers characteristic of yolk sac, such as cytokeratin 19 and extracellular matrix proteins, but none of the secreted serum proteins produced by normal yolk sac or liver. HNF-3 alpha expression increased upon retinoic acid-induced GCT 27 X-1 differentiation. This increase in HNF-3 alpha expression may characterize an early stage in the differentiation of extraembryonic endoderm. In support of this hypothesis, we found that a yolk sac carcinoma cell line with a phenotype similar to rodent visceral endoderm expressed transcripts for HNF-1 alpha, -1 beta, -3 alpha, -3 beta, -3 gamma, and 4, whereas yolk sac carcinoma cell lines resembling rodent parietal endoderm expressed transcripts for HNF-3 alpha. The results support the conclusion that hepatocytic transcription factors, particularly HNF-3 alpha, may play an important role in early endodermal differentiation in man.

Animals↗
PubMed1997

Formation of reticulated endoderm, Reichert's membrane, and amniogenesis in blastocysts of captive-bred, short-tailed fruit bats, Carollia perspicillata.

BACKGROUND AND METHODS: As part of an effort to develop the short-tailed fruit bat (Carollia perspicillata) as a new animal model for the study of interstitial implantation and trophoblast-uterine interactions, early embryogenesis was examined histologically and ultrastructurally in captive-bred females at different intervals after the first appearance of spermatozoa in daily vaginal smears (day 1 postcoitum [p.c.]). RESULTS: In most of the early uterine embryos examined on days 16-18 p.c., much of the endoderm appeared as a reticulated meshwork; however, a unilocular yolk sac was formed prior to the development of any mesoderm. Early blastocysts of Carollia were also unusual in that endoderm surrounded much of the inner cell mass (ICM), Reichert's membrane continued over the dorsal side of the ICM, and basal laminalike material was observed around many of the endoderm and epiblast cells. A primordial amniotic cavity was formed between days 19 and 26 p.c. by cavitation. The first mesoderm appeared between days 23 and 26 p.c., concommitant with the development of an embryonic shield. CONCLUSION: The unusual reticulated appearance of early endoderm in Carollia, which is reminiscent of that seen in early human blastocysts, may be attributable to constraints imposed on growth of the blastocyst by the site and mode of implantation, temporary retardation of trophoblastic invasion by the basal laminae of endometrial epithelial elements, and endodermal proliferation in anticipation of rapid yolk sac expansion. Reichert's membrane appears to play an important role in this species in tethering the ICM and embryonic shield to the developing placenta prior to the formation of significant amounts of mesoderm.

Amnion↗
PubMed1976

Cytological development of yolk sac endoderm and protein-absorptive mesothelium in the little brown bat, Myotis lucifugus.

The yolk sac of the little brown bat is unusual in that during the course of gestation both the inner endodermal cells (bordering the yolk sac cavity) and outer mesothelium (facing the exocelom) form simple columnar epithelia which persist throughout gestation. These endodermal cells develop an extensive system of agranular endoplasmic reticulum, numerous lipid droplets and unusual "giant" mitochondria. During development the Golgi apparatus changes position from the apical to the basal side of the nucleus, reversing the polarity of the cells. In general, the endodermal cells have cytological features suggestive of synthetic or secretory activity. The mesothelial cells develop an extensive "absorptive apparatus" in their apices, while large crystalloid-containing granules become numerous in their basal cytoplasm. The mesothelial cells have large deposits of glycogen, especially during mid-gestation, but few mitochondria and little granular endoplasmic reticulum. Endodermal cells do not absorb exogenous protein (peroxidase) even if it is injected directly into the yolk sac cavity. However, placement of peroxidase either in the exocelom or in the maternal vascular system results in the appearance of this protein in the "absorptive apparatus" of mesothelial cells as well as in macrophages in the stroma of the yolk sac. While evidence of absorption was clear, no direct evidence of transport of tracer to fetal blood vascular system was obtained. It is postulated that a major function of the hypertrophied mesothelial cells during gestation is the absorption of proteins and possibly other substances from the exocelomic fluid. The major function of the hypertrophied endodermal cells may be synthesis and secretion of substances into the fetal circulation.

Animals↗
PubMed1983

A fine structural and cytochemical study of the rhesus monkey yolk sac: endoderm and mesothelium.

This study has examined the fine structure and some cytochemical characteristics of the endodermal and mesothelial cells of the rhesus monkey yolk sac between 25 and 66 days of gestation. The endodermal cells were characterized by abundant granular endoplasmic reticulum, some agranular endoplasmic reticulum, a well-developed Golgi apparatus, and numerous large mitochondria. During the earlier part of the period studied, endodermal cells had a few acid phosphatase and arylsulfatase-positive lysosomes and moderate numbers of catalase-positive microperoxisomes. During the later stages of development, large granules (believed to be lysosomes) with a heterogeneous content were numerous in the cytoplasm. Mesothelial cells showed fewer development changes. Throughout this period they were usually flattened cells with long microvilli, small mitochondria, and limited amounts of granular endoplasmic reticulum. The mesothelial cells had acid phosphatase reaction product in the Golgi region and occasional large vesicles, but were negative for arylsulfatase and catalase. One specimen was incubated at 37 degrees C in the presence of horseradish peroxidase in order to examine endocytosis. Both the mesothelial cells and endodermal cells internalized the peroxidase into a variety of cytoplasmic vesicles. Based on their cytology, the endodermal cells may function in the synthesis of serum proteins during this period, as has been suggested in other species. They may also be involved in lipid metabolism. The mesothelial cells appeared less synthetically active, but evidence suggested that they may be involved in collagen and extracellular matrix production. The endocytic activity displayed by both cell types may indicate a role in fluid and metabolite transfer across the epithelia. The cytology of both cell types was very similar to that described for human yolk sacs, suggesting that the rhesus monkey may be a useful species in which to study the maturation of yolk sac function.

Animals↗
PubMed1993

Natural wound formation: endodermal responses in experimental primary neural induction in the chick embryo.

Natural wound formation in experimental primary neural induction has been studied by SEM and in paraffin wax sections in embryos from 0 minutes to 10 hours of re-incubation. Stage 4 host and graft embryos were removed from hen's eggs and mounted as for New culture. Graft Hensen's nodes were transplanted into "pockets" created in the host area pellucida and re-incubated for up to 10 hours. Initially the cut edges of the graft establish contact with the host ectoderm layer. After 4 hours the cut edges of the graft move from the host ectoderm to the host endoderm layer. Several small openings form in the host endoderm over the graft tissue. By 6 hours, these openings join to form a single natural wound through which the underlying graft is exposed to the external environment. At 8 hours the graft forms a head-fold and neural folds are evident. During 8 to 10 hours of re-incubation the edges of the graft which attach to the edges of the host endoderm meet in the midline and close the opening in the host endoderm; simultaneously, the graft forms a neural tube. The endodermal wounds form by cell re-arrangement and by a minor contribution from cell loss.

Animals↗
PubMed2003

Mouse Mix gene is activated early during differentiation of ES and F9 stem cells and induces endoderm in frog embryos.

In frog and zebrafish, the Mix/Bix family of paired type homeodomain proteins play key roles in specification and differentiation of mesendoderm. However, in mouse, only a single Mix gene (mMix) has been identified to date and its function is unknown. We have analyzed the expression of mouse Mix RNA and protein in embryos, embryoid bodies formed from embryonic stem cells and F9 teratocarcinoma cells, as well as several differentiated cell types. Expression in embryoid bodies in culture mirrors that in embryos, where Mix is transcribed transiently in primitive (visceral) endoderm (VE) and in nascent mesoderm. In F9 cells induced by retinoic acid to differentiate to VE, mMix is coordinately expressed with three other endodermal transcription factors, well before AFP, and its protein product is localized to the nucleus. In a subpopulation of nascent mesodermal cells from embryonic stem cell embryoid bodies, mMix is coexpressed with Brachyury. Intriguingly, mMix mRNA is detected in a population (T+Flk1+) of cells which may contain hemangioblasts, before the onset of hematopoiesis and activation of hematopoietic markers. In vitro and in vivo, mMix expression in nascent mesoderm is rapidly down-regulated and becomes undetectable in differentiated cell types. In the region of the developing gut, mMix expression is confined to the mesoderm of mid- and hindgut but is absent from definitive endoderm. Injection of mouse mMix RNA into early frog embryos results in axial truncation of developing tadpoles and, in animal cap assays, mMix alone is sufficient to activate expression of several endodermal (but not mesodermal) markers. Although these observations do not exclude a possible cell-autonomous function for mMix in mesendodermal progenitor cells, they do suggest an additional, non-cell autonomous role in nascent mesoderm in the formation and/or patterning of adjacent definitive endoderm.

Animals↗
PubMed2006

Definitive endoderm of the mouse embryo: formation, cell fates, and morphogenetic function.

The endoderm is one of the primary germ layers but, in comparison to ectoderm and mesoderm, has received less attention. The definitive endoderm forms during gastrulation and replaces the extraembryonic visceral endoderm. It participates in the complex morphogenesis of the gut tube and contributes to the associated visceral organs. This review highlights the role of the definitive endoderm as a source of patterning cues for the morphogenesis of other germ-layer tissues, such as the anterior neurectoderm and the pharyngeal region, and also emphasizes the intricate patterning that the endoderm itself undergoes enabling the acquisition of regionalized cell fates.

Animals↗
PubMed2006

Visceral endoderm function is regulated by quaking and required for vascular development.

The quaking (qkI) gene produces three major alternatively spliced variants (qkI-5,-6,-7) that encode for proteins that share the RNA binding, KH domain. Previous studies utilizing the qk(k2) allele, which contains an N-ethyl-N-nitrosourea (ENU)-induced point mutation in the KH domain, demonstrate that this functional region of qkI is required for embryonic vascular development. In the current studies we demonstrate that qk(l-1)/qk(l-1) mutants, which lack the QKI-5 splice variant, also died at midgestation due to vascular remodeling defects. In addition, although all three QKI isoforms were expressed in the visceral endoderm of wildtype yolk sacs, qkI-6 and qkI-7 transcript and protein expression were suppressed in qk(k2)/qk(k2) and qk(l-1)/qk(l-1) mutant yolk sacs, suggesting that the KH-domain of QKI-5 was required for qkI-6 and qkI-7 expression. Further studies revealed that the cellular role of qkI is to regulate visceral endoderm function, including the local synthesis of retinoic acid (RA) and the subsequent control of endothelial cell proliferation, matrix production, and visceral endoderm survival. Although these defects were rescued by exogenous RA, visceral endoderm function or vascular remodeling were not restored. Thus, we conclude that qkI regulates visceral endoderm function, which is critical for vascular remodeling.

Animals↗
PubMed1983

Parietal and visceral endoderm differ in their expression of intermediate filaments.

Two layers of extra-embryonic endoderm, viz. the parietal endoderm (PE) and the visceral endoderm (VE), arise in the mouse embryo shortly after implantation. Both cell populations apparently originate from the primitive endoderm of the blastocyst. While the endoderm differentiation has been studied both in the embryo and in the embryonal carcinoma model system, the investigation has been hampered by the paucity of unequivocal markers of differentiation, especially in the case of the PE. Here we show that the PE and VE of mouse conceptuses differ in their expression of intermediate filaments: while both cell types contain cytokeratin, expression of vimentin was only revealed in the cells of the PE. The association between the differentiation of PE and the appearance of vimentin filaments is discussed.

Animals↗
PubMed2006

Endodermal differentiation of murine embryonic carcinoma cells by retinoic acid requires JLP, a JNK-scaffolding protein.

Retinoic acid (RA) is a morphogen that induces endodermal differentiation of murine P19 embryonic carcinoma cells. RA-induced differentiation of P19 cells has been used as a model system to define the differentiation programs of pluripotent stem cells. Using this system it has been shown that G alpha13--the alpha-subunit of the heterotrimeric G protein G13--and its activation of JNK-module are critically required for the endodermal differentiation of P19 cells. However, the mechanism through which G alpha13 is linked to JNK-module is unknown. Here, we report that RA stimulates the expression of JNK-interacting leucine zipper protein (JLP), a newly identified JNK-scaffolding protein and its critical role in RA-mediated endodermal differentiation. Our results indicate that there is a physical association between JLP and G alpha13 in RA-stimulated P19 cells. More interestingly, silencing JLP abrogates RA-mediated endodermal differentiation of P19 cells analogous to the effects seen with the silencing of G alpha13 or JNK. Therefore, our studies presented here identify for the first time, a novel role for a newly identified scaffolding protein in RA-mediated endodermal differentiation, providing a new signaling conduit to transmit signals from RA to JNK module.

Adaptor Proteins, Signal Transducing↗
PubMed1985

Production of insulin-like growth factor-II (MSA) by endoderm-like cells derived from embryonal carcinoma cells: possible mediator of embryonic cell growth.

The present study was carried out to determine if an insulin-like growth factor (IGF) type activity might be produced by embryonal carcinoma-derived cells. The cell line used to condition growth medium for the isolation of secreted growth factors was a newly established Dif 5 cell type. Dif 5 cells are a differentiated endoderm-like cell type derived from F9 embryonal carcinoma cells (which possess properties similar to mouse embryonic stem cells) following extensive exposure to retinoic acid. When growth medium conditioned by Dif 5 cells is chromatographed on Sephadex G-75 in 1 M acetic acid two peaks of activity are observed which compete for specific [125I]iodo multiplication stimulating activity (MSA) binding to PYS cells. MSA is the rat homologue of human IGF-II. The high molecular weight fraction (Mr approximately 60K) apparently corresponds to IGF-binding protein as determined by its ability to bind [125I]iodo-MSA. The low molecular weight fraction (Mr approximately 8K) is biologically active as this fraction stimulates [3H]thymidine incorporation into serum-starved chick embryo fibroblasts. Radioimmunoassay data indicate that the IGF-like activity produced by Dif 5 cells is more closely related to IGF-II than to IGF-I. Undifferentiated embryonal carcinoma stem cell lines (F9, Nulli, and PCC4) produced little of this MSA-like activity, while PYS-2 (parietal endoderm-like) cells produced about 16 ng MSA/10(6) cells/24 hr as determined by radioimmunoassay. Dif 5 and PSA-5E (visceral endoderm-like) cells, are found to secrete significant amounts of MSA into the growth medium (30-50 ng MSA/10(6) cells/24 hr). These findings offer further support to a proposal that MSA (IGF-II) produced by endoderm cells, particularly visceral endoderm, may serve as an early embryonic growth factor.

Animals↗
PubMed1977

Segregation during cleavage of a factor determining endodermal alkaline phosphatase development in ascidian embryos.

Localized alkaline phosphatase activity (EC 3.1.3.1) develops progressively in endodermal tissues of the presumptive digestive system in Ciona intestinalis embryos. It was first detected histochemically at late gastrulation, and a puromycin sensitivity period coincident with this time suggests that new alkaline phosphatase is synthesized. Embryos in which cell division was blocked with cytochalasin B at early cleavage stages up to the 64-cell stage, eventually differentiated strong alkaline phosphatase activity in certain cells at each cleavage-arrested stage. The maximum cell numbers and their positions were identical to those of the previously known endodermal cell lineage. Actinomycin D did not prevent development of endodermal alkaline phosphatase when administered from fertilization onwards, nor did other inhibitors of RNA synthesis (chromomycin A3, cordycepin, and daunomycin). There is probably a preformed maternal mRNA for endodermal alkaline phosphatase present in the unfertilizec Ciona egg. Either this RNA itself, or some related translation factor, is localized in the egg cytoplasm and segregated during early cleavages into the endodermal cell lineage of the embryo.

Acetylcholinesterase↗
PubMed1984

Metabolic activation of cyclophosphamide by yolk sac endodermal cells of the early chick embryo.

Endodermal cells isolated from the yolk sacs of day 3 chick embryos were able to activate metabolically cyclophosphamide. This was demonstrated by the cytotoxicity of cyclophosphamide to the endodermal cells themselves as well as by the ability of endodermal tissue to mediate a cytotoxic response in coculture with KB cells, a human tumor cell line unable to activate cyclophosphamide. Yolk sac endodermal cells from day 3 embryos were sensitive to cyclophosphamide when the drug was added immediately after the start of culture, but not when the drug was added after 24 hr of culture. The ability to metabolize cyclophosphamide by the day 3 embryo appeared limited to the endodermal cells of the yolk sac as cells derived from neither the embryo proper nor yolk sac mesoderm-ectoderm tissue were positive in these tests. Using whole blastoderms, cyclophosphamide activation was detected as early as 12 hr of egg incubation.

Animals↗
PubMed1995

Activin-A and FGF-2 mimic the inductive effects of anterior endoderm on terminal cardiac myogenesis in vitro.

We recently reported that the differentiation of cultured embryonic precardiac myocytes is specifically promoted by anterior lateral plate endoderm from Hamburger-Hamilton stage 6 chick embryos. Polypeptide growth factors are probable mediators of cardiogenesis during embryonic development. It was previously noted that activin-A is a major secretory product of endoderm cultured from chicken embryos. Also, fibroblast growth factor-like proteins are present in anterior endoderm of stage 6 chick embryos. Therefore, we have examined the cardiogenic effects of these growth factors on cultured precardiac mesoderm cells explanted from stage 6 embryos. Similar to the effects of anterior endoderm, low concentrations of activin-A, FGF-2 (bFGF), or insulin significantly increased the incidence of explants that exhibited synchronous contractions and expressed cardiac alpha-actin mRNA. By contrast, explants treated with transferrin, bovine serum albumin, or nerve growth factor never contracted and contained only cytoplasmic beta-actin transcripts. These results provide additional evidence that endoderm-secreted activin-A, FGF-2, and perhaps insulin participate in regulating terminal cardiac differentiation in the embryo.

Actins↗
PubMed1996

Expression of avian Pax1 and Pax9 is intrinsically regulated in the pharyngeal endoderm, but depends on environmental influences in the paraxial mesoderm.

Pax1 and Pax9 represent a subfamily of paired-box-containing genes. In vertebrates, Pax1 and Pax9 transcripts have been found specifically in mesodermal tissues and the pharyngeal endoderm. Pax1 expression in the sclerotomes has been shown to be indispensable for proper formation of the axial skeleton, but expression of Pax1 in the endoderm has not been studied in detail. We have cloned the chick homologue of the murine Pax9 gene. Our results show that transcripts of Pax1 and Pax9 are first detectable in the prospective foregut endoderm of headfold-stage avian embryos. Endodermal expression correlates with the highly proliferative zones of the folding foregut and evaginating pharyngeal pouches. In later stages, Pax1 and Pax9 are expressed in overlapping but distinct patterns within the developing sclerotomes and limb buds. From grafting experiments we conclude that activation of pharyngeal Pax1 and Pax9 expression is an intrinsic property of the endoderm, not requiring midline structures or head mesoderm. In contrast, notochord is required to induce Pax1 in competent sclerotomes. Here we show that in vitro there is a cranio-caudal gradient of inductive capacity in the notochord. This coincides with the graded expression of Pax1 and Pax9 along the cranio-caudal axis in 2- to 3-day-old embryos. Furthermore, paraxial head mesoderm shows no competence to express Pax1. Finally, in vitro we find counteracting influences on notochord signaling by lateral tissues (lateral plate, intermediate mesoderm), leading to an inhibition of Sonic hedgehog (Shh) expression in notochord and floor plate, as well as Pax1 and Pax9 expression in sclerotomes. Taken together, our results demonstrate that different mechanisms regulate expression of Pax1 and Pax9 in foregut and sclerotome, but suggest a common function for both genes in the two tissues that is promoting proliferation and preventing fusion of neighboring blastemas.

Amino Acid Sequence↗
PubMed1997

Wild-type endoderm abrogates the ventral developmental defects associated with GATA-4 deficiency in the mouse.

GATA-4 knockout mice die by 9.5 days postcoitum and exhibit profound defects in ventral morphogenesis, including abnormal foregut formation and a failure of fusion of the bilateral myocardial primordia. During early mouse development, GATA-4 is expressed in cardiogenic splanchnic mesoderm and associated endoderm, suggesting that the presence of this transcription factor in one or both of these tissue types is essential for ventral development. To distinguish whether GATA-4 expression in mesoderm or endoderm accounts for the phenotype of the knockout mouse, we prepared chimeric mice by injecting Gata4-/- ES cells into 8-cell stage ROSA26(Gata4+/+) embryos. We identified a series of high percentage null chimeras (8-10 days postcoitum) in which Gata4+/+ cells were restricted to visceral yolk sac endoderm and small portions of the foregut/hindgut endoderm. Despite an absence of GATA-4 in all other cells of these embryos, there was normal development of the heart, foregut, and surrounding tissues. We conclude that expression of GATA-4 in endoderm rather than cardiogenic mesoderm is required for ventral morphogenesis.

Animals↗