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At least 289 records · Page 16Linked to original sources
PubMed2000

Development of chick axial mesoderm: specification of prechordal mesoderm by anterior endoderm-derived TGFbeta family signalling.

Two populations of axial mesoderm cells can be recognised in the chick embryo, posterior notochord and anterior prechordal mesoderm. We have examined the cellular and molecular events that govern the specification of prechordal mesoderm. We report that notochord and prechordal mesoderm cells are intermingled and share expression of many markers as they initially extend out of Hensen's node. In vitro culture studies, together with in vivo grafting experiments, reveal that early extending axial mesoderm cells are labile and that their character may be defined subsequently through signals that derive from anterior endodermal tissues. Anterior endoderm elicits aspects of prechordal mesoderm identity in extending axial mesoderm by repressing notochord characteristics, briefly maintaining gsc expression and inducing BMP7 expression. Together these experiments suggest that, in vivo, signalling by anterior endoderm may determine the extent of prechordal mesoderm. The transforming growth factor (beta) (TGFbeta) superfamily members BMP2, BMP4, BMP7 and activin, all of which are transiently expressed in anterior endoderm mimic distinct aspects of its patterning actions. Together our results suggest that anterior endoderm-derived TGFbetas may specify prechordal mesoderm character in chick axial mesoderm.

Activins↗
PubMed2000

Endoderm patterning by the notochord: development of the hypochord in Xenopus.

The patterning and differentiation of the vertebrate endoderm requires signaling from adjacent tissues. In this report, we demonstrate that signals from the notochord are critical for the development of the hypochord, which is a transient, endodermally derived structure that lies immediately ventral to the notochord in the amphibian and fish embryo. It appears likely that the hypochord is required for the formation of the dorsal aorta in these organisms. We show that removal of the notochord during early neurulation leads to the complete failure of hypochord development and to the elimination of expression of the hypochord marker, VEGF. Removal of the notochord during late neurulation, however, does not interfere with hypochord formation. These results suggest that signals arising in the notochord instruct cells in the underlying endoderm to take on a hypochord fate during early neural stages, and that the hypochord does not depend on further notochord signals for maintenance. In reciprocal experiments, when the endoderm receives excess notochord signaling, a significantly enlarged hypochord develops. Overall, these results demonstrate that, in addition to patterning neural and mesodermal tissues, the notochord plays an important role in patterning of the endoderm.

Animals↗
PubMed2001

Otx2 is required for visceral endoderm movement and for the restriction of posterior signals in the epiblast of the mouse embryo.

Genetic and embryological experiments have demonstrated an essential role for the visceral endoderm in the formation of the forebrain; however, the precise molecular and cellular mechanisms of this requirement are poorly understood. We have performed lineage tracing in combination with molecular marker studies to follow morphogenetic movements and cell fates before and during gastrulation in embryos mutant for the homeobox gene Otx2. Our results show, first, that Otx2 is not required for proliferation of the visceral endoderm, but is essential for anteriorly directed morphogenetic movement. Second, molecules that are normally expressed in the anterior visceral endoderm, such as Lefty1 and Mdkk1, are not expressed in Otx2 mutants. These secreted proteins have been reported to antagonise, respectively, the activities of Nodal and Wnt signals, which have a role in regulating primitive streak formation. The visceral endoderm defects of the Otx2 mutants are associated with abnormal expression of primitive streak markers in the epiblast, suggesting that anterior epiblast cells acquire primitive streak characteristics. Taken together, our data support a model whereby Otx2 functions in the anterior visceral endoderm to influence the ability of the adjacent epiblast cells to differentiate into anterior neurectoderm, indirectly, by preventing them from coming under the influence of posterior signals that regulate primitive streak formation.

Animals↗
PubMed2002

Requirement for endoderm and FGF3 in ventral head skeleton formation.

The vertebrate head skeleton is derived in part from neural crest cells, which physically interact with head ectoderm, mesoderm and endoderm to shape the pharyngeal arches. The cellular and molecular nature of these interactions is poorly understood, and we explore here the function of endoderm in this process. By genetic ablation and reintroduction of endoderm in zebrafish, we show that it is required for the development of chondrogenic neural crest cells, including their identity, survival and differentiation into arch cartilages. Using a genetic interference approach, we further identify Fgf3 as a critical component of endodermal function that allows the development of posterior arch cartilages. Together, our results reveal for the first time that the endoderm provides differential cues along the anteroposterior axis to control ventral head skeleton development and demonstrate that this function is mediated in part by Fgf3.

Animals↗
PubMed1987

Induction of myofibrillogenesis in cardiac lethal mutant axolotl hearts rescued by RNA derived from normal endoderm.

A strain of axolotl, Ambystoma mexicanum, that carries the cardiac lethal or c gene presents an excellent model system in which to study inductive interactions during heart development. Embryos homozygous for gene c contain hearts that fail to beat and do not form sarcomeric myofibrils even though muscle proteins are present. Although they can survive for approximately three weeks, mutant embryos inevitably die due to lack of circulation. Embryonic axolotl hearts can be maintained easily in organ culture using only Holtfreter's solution as a culture medium. Mutant hearts can be induced to differentiate in vitro into functional cardiac muscle containing sarcomeric myofibrils by coculturing the mutant heart tube with anterior endoderm from a normal embryo. The induction of muscle differentiation can also be mediated through organ culture of mutant heart tubes in medium 'conditioned' by normal anterior endoderm. Ribonuclease was shown to abolish the ability of endoderm-conditioned medium to induce cardiac muscle differentiation. The addition of RNA extracted from normal early embryonic anterior endoderm to organ cultures of mutant hearts stimulated the differentiation of these tissues into contractile cardiac muscle containing well-organized sarcomeric myofibrils, while RNA extracted from early embryonic liver or neural tube did not induce either muscular contraction or myofibrillogenesis. Thus, RNA from anterior endoderm of normal embryos induces myofibrillogenesis and the development of contractile activity in mutant hearts, thereby correcting the genetic defect.

Ambystoma↗
PubMed1999

Volume of liquid below the epithelium of an F9 cell as a signal for differentiation into visceral endoderm.

When retinoic acid-primed F9 cells are allowed to aggregate, they form embryoid bodies with an outer layer of (&agr;)-fetoprotein-producing visceral endoderm cells and an internal cavity. I show that maturation of the visceral endoderm is dependent on the size of F9 aggregates. Size fractionation of aggregates of retinoic acid-primed F9 cells on Percoll density gradients revealed that only aggregates with diameters larger than 180 microm developed into embryoid bodies with an endoderm layer secreting (&agr;)-fetoprotein. Size dependent alpha-fetoprotein-secretion was also observed when retinoic acid-primed F9 cells were cultured on porous microcarrier beads larger than 185 microm. Retinoic acid-primed F9 cells on flat microporous membranes did not differentiate and secrete alpha-fetoprotein unless exposed to a limited volume of medium at their basolateral surface. This suggested that maturation of the visceral endoderm is signaled by the volume of liquid phase below the epithelium. I postulate that the epithelial layer of an F9 aggregate encloses liquid and forms a barrier to diffusion of some critical factor(s). The concentration of such a factor may reach a threshold due to enlargement of the liquid phase during growth of the F9 aggregate and thereby signal maturation of the outer layer of cells into visceral endoderm.

Animals↗
PubMed2004

An integrin-dependent role of pouch endoderm in hyoid cartilage development.

Pharyngeal endoderm is essential for and can reprogram development of the head skeleton. Here we investigate the roles of specific endodermal structures in regulating craniofacial development. We have isolated an integrinalpha5 mutant in zebrafish that has region-specific losses of facial cartilages derived from hyoid neural crest cells. In addition, the cranial muscles that normally attach to the affected cartilage region and their associated nerve are secondarily reduced in integrinalpha5- animals. Earlier in development, integrinalpha5 mutants also have specific defects in the formation of the first pouch, an outpocketing of the pharyngeal endoderm. By fate mapping, we show that the cartilage regions that are lost in integrinalpha5 mutants develop from neural crest cells directly adjacent to the first pouch in wild-type animals. Furthermore, we demonstrate that Integrinalpha5 functions in the endoderm to control pouch formation and cartilage development. Time-lapse recordings suggest that the first pouch promotes region-specific cartilage development by regulating the local compaction and survival of skeletogenic neural crest cells. Thus, our results reveal a hierarchy of tissue interactions, at the top of which is the first endodermal pouch, which locally coordinates the development of multiple tissues in a specific region of the vertebrate face. Lastly, we discuss the implications of a mosaic assembly of the facial skeleton for the evolution of ray-finned fish.

Animals↗
PubMed1999

Head-organizing activities of endodermal tissues in vertebrates.

The embryonic organizer represents the major regulatory centre for the establishment of the body axes during gastrulation. Here, we discuss the endodermal contributions to the organizer of amphibia, birds and mammals. We differentiate between the definitive, prospective liver endoderm, and the primitive, prospective extraembryonic endoderm, the latter addressed as the hypoblast in birds and the visceral endoderm in mammals. We further discuss the role of the prechordal plate, a mesendodermal tissue underlying the prospective forebrain. Our conclusion points out the similarity of the amphibian and the avian organizer, with a concentration of inductive potentials in time and space. On the other hand, we discuss the unique feature of mammals, that have shifted certain aspects of the head organizer into the anterior visceral endoderm.

Amphibians↗
PubMed2000

Snail is an immediate early target gene of parathyroid hormone related peptide signaling in parietal endoderm formation.

In mouse development, parietal endoderm (PE) is formed from both primitive endoderm (PrE) and visceral endoderm (VE). This process can be mimicked in vitro by using F9 embryonal carcinoma cells (EC) cells, differentiated to PrE or VE cells, and treating these with Parathyroid Hormone related Peptide (PTHrP). By means of differential display RT-PCR, we identified Snail (Sna) as a gene upregulated during the differentiation from F9 PrE to PE. We show that Sna is an immediate early target gene of PTHrP action in the formation of F9 PE cells. Using RT-PCR, we detected Sna transcripts in pre-implantation mouse embryos from the zygote-stage onwards. Sna was strongly upregulated in parallel with type 1 PTH/PTHrP Receptor (PTH(rP)-R1) mRNA in mouse blastocysts plated in culture, concomitant with detection of the PE-marker Follistatin and appearance of PE cells. By radioactive in situ hybridization on sections of mouse embryos, we found Sna expression in the earliest PE cells at E5.5. Sna remained expressed until at least E7.5. At this stage, we also observed clear expression in endoderm cells delaminating from the epithelial sheet of VE cells in the marginal zone. We conclude that PTH(rP)-R1 and Sna are expressed in endodermal cells that change from an epithelial to a mesenchymal phenotype. Since Sna expression has been described at other sites where epithelio-mesenchymal transitions (EMT) occur, such as the primitive streak at gastrulation and in pre-migratory neural crest cells, we hypothesize that Sna is instrumental in the action of PTHrP inducing PE formation, which we propose to be the first EMT in mouse development.

Animals↗
PubMedDate not supplied

Endodermal cyst in the cerebellopontine angle with immunohistochemical reactivity for CA19-9.

We present a rare case of the endodermal cyst in the cerebellopontine angle with positive immunohistochemical reactivity for CA19-9. The patient was a 67-year-old woman with an endodermal cyst in the cerebellopontine angle who presented with progressive gait disturbance. A magnetic resonance image showed a cerebellopontine angle which was low in signal on T1-weighted, and high on T2-weighted image without gadolinium enhancement. The preoperative diagnosis was an epidermoid or arachnoid cyst. The patient underwent surgery. Since the intraoperative histological diagnosis by frozen section was endodermal cyst, total removal of the cyst wall was achieved for preventing recurrence. The postoperative definitive histological diagnosis was endodermal cyst, type A by Wilkins-Odom classification, lined by mucinous epithelium with an immunohistochemical reactivity for CA 19-9 protein and cytokeratin. This is the first reported case of a huge endodermal cyst in the cerebellopontine angle of an elderly woman which exclusively showed a differentiation toward the midgut epithelium. The histological diagnosis during surgery by frozen section should be performed for proper treatment.

Aged↗
PubMed2002

New perspectives on therapy for vaginal endodermal sinus tumors.

PURPOSE: Malignant germ cell tumors account for 3% of childhood cancers. Endodermal sinus tumor, the most common malignant germ cell tumor, requires treatment primarily with chemotherapy and surgery is reserved as a last resort. It is rare for the vagina to be the primary site of endodermal sinus tumor, and we report on our experiences with this phenomenon at a single institution. MATERIALS AND METHODS: We retrospectively reviewed the clinical features, treatment and outcomes of 3 children with vaginal endodermal sinus tumor. RESULTS: Initial treatment was combination chemotherapy, in 2 patients. alpha-fetoprotein decreased rapidly and returned to normal in both. One patient is disease-free 7 years after chemotherapy and the other patient is currently disease-free with a normal alpha-fetoprotein 3 months after induction chemotherapy. In the remaining case progressive disease developed following initial chemotherapy and subsequent salvage surgery combined with radiation, chemotherapy and ultimately autologous bone marrow transplant was performed. The patient has remained disease-free for 6.5 years since completing this extensive therapy. CONCLUSIONS: Endodermal sinus tumor of the vagina is rare. All of our patients presented with painless bleeding of no obvious source. In such cases one must maintain a high index of suspicion for possible underlying pathological conditions even if ultrasound is negative. Evaluation must include endoscopic examination of the lower genitourinary tract. Bone marrow transplant should be considered as a last therapeutic resort in salvage cases of unresponsive vaginal endodermal sinus tumor.

Combined Modality Therapy↗
PubMed1988

Ultrastructural pathologic changes of rat extraembryonic visceral endodermal cells exposed to teratogenic antibodies in vivo.

It has been well established that certain heterologous tissue antibodies may induce abnormal embryonic development when injected into pregnant rodents during the organogenetic period. It has been postulated that these antibodies indirectly cause embryopathy by interfering with the normal functions of the yolk-sac placenta. The exact mechanism whereby these antibodies may induce placental pathology is not known. Specific teratogenic antibodies against a homogeneous rat kidney glycoprotein or a visceral yolk-sac glycoprotein antigen were injected intraperitoneally into 9th day pregnant rats. Electron microscopic examinations of the extraembryonic visceral endodermal cells of the egg cylinder were performed at 4, 6, 9, and 24 hours after the administration of the teratogenic antibodies. Control animals were injected with normal rabbit serum proteins. Extraembryonic visceral endodermal cells were similarly processed and examined as the experimental groups. The results seemed to indicate that the teratogenic antibodies induced increased autophagocytosis and morphologic changes associated with the phagolysosomes (secondary lysosomes) within the extraembryonic visceral endodermal cells at 9 hours following antibody administration. After 24 hours there was an apparent reduction or a complete disappearance of the supranuclear phagolysosome-like and lysosome-like structures, and the appearance of many large and small electron lucent vacuoles containing finely granular materials. Similar ultrastructural pathology was not observed in the 4 and 6 hour experimental and all of the control groups of animals. No other obvious intracellular or intercellular changes were observed in all of the experimental groups. Although the exact mechanism whereby the teratogenic antibodies may induce pathologic changes in the extraembryonic visceral endodermal cells remains to be determined, the present ultrastructural study demonstrated, for the first time, that teratogenic antibodies induced abnormal pathology in the extraembryonic visceral endodermal cells during the critical period of organogenesis.

Animals↗
PubMed1994

Murine yolk sac endoderm- and mesoderm-derived cell lines support in vitro growth and differentiation of hematopoietic cells.

The mechanisms involved in the induction of yolk sac mesoderm into blood islands and the role of visceral endoderm and mesoderm cells in regulating the restricted differentiation and proliferation of hematopoietic cells in the yolk sac remain largely unexplored. To better define the role of murine yolk sac microenvironment cells in supporting hematopoiesis, we established cell lines from day-9.5 gestation murine yolk sac visceral endoderm and mesoderm layers using a recombinant retrovirus vector containing Simian virus 40 large T-antigen cDNA. Obtained immortalized cell lines expressed morphologic and biosynthetic features characteristic of endoderm and mesoderm cells from freshly isolated yolk sacs. Similar to the differentiation of blood island hematopoietic cells in situ, differentiation of hematopoietic progenitor cells in vitro into neutrophils was restricted and macrophage production increased when bone marrow (BM) progenitor cells were cultured in direct contact with immortalized yolk sac cell lines as compared with culture on adult BM stromal cell lines. Yolk sac-derived cell lines also significantly stimulated the proliferation of hematopoietic progenitor cells compared with the adult BM stromal cell lines. Thus, yolk sac endoderm- and mesoderm-derived cells, expressing many features of normal yolk sac cells, alter the growth and differentiation of hematopoietic progenitor cells. These cells will prove useful in examining the cellular interactions between yolk sac endoderm and mesoderm involved in early hematopoietic stem cell proliferation and differentiation.

Animals↗
PubMed1996

Endoderm induction by the organizer-secreted factors chordin and noggin in Xenopus animal caps.

Spemann's organizer has potent neural inducing and mesoderm dorsalizing activities in the Xenopus gastrula. A third activity, the organizer's ability to induce a secondary gut, has been difficult to analyze experimentally due to the lack of early gene markers. Here we introduce endodermin, a pan-endodermal gene marker, and use it to demonstrate that chordin (Chd), a protein secreted by the organizer region, is able to induce endodermal differentiation in Xenopus. The ability of chd, as well as that of noggin, to induce endoderm in animal cap explants is repressed by the ventralizing factor BMP-4. When FGF signaling is blocked by a dominant-negative FGF receptor in chd-injected animal caps, neural induction is inhibited and most of the explant is induced to become endoderm. The results suggest that proteins secreted by the organizer, acting together with known peptide growth factors, regulate differentiation of the endodermal germ layer.

Amino Acid Sequence↗
PubMed1976

Endodermal sinus tumour of the ovary: a comparative light and electron microscopic study.

An endodermal sinus tumour of the ovary from a 12 year old girl is analysed light- and electron microscopically. The histological appearance is characterized by glandular-papillary structures and microcystic-reticular areas with inclusion of occasional endodermal sinuses. By electron microscopy immature and highly differentiated cells can be distinguished. In analogy to certain structures in the human yolk sac the most differentiated cells in the tumour are regarded as neoplastic endoderm. On the basis of transitional forms between immature and differentiated cells a development of the latter from the former is suggested. The cells in mesenchyme-like areas differ from those of solid and glandular parts merely in the degree of cytoplasmic differentiation but are otherwise believed to represent the same "cell line". In addition to other possible cell functions the cytoplasmic features of the differentiated cell indicates a protein synthesis and secretion. From our observations it is concluded that the endodermal sinus tumour originates from germ cells and differentiates into yolk sac endoderm. The ultrastructural differences between this tumour and clear cell carcinomas of the ovary are discussed.

Cell Membrane↗
PubMed1990

Germ cell neoplasms of head and neck soft tissues: a pathologic spectrum of teratomatous and endodermal sinus tumors.

Germ-cell neoplasms, in particular teratomas with immature and mature somatic type tissues, are some of the most commonly found tumors in children. Approximately 5% of these neoplasms appear in one of several extracranial sites in the head and neck region. This study reports the clinical, pathologic and immunohistochemical findings in six germ-cell neoplasms occurring in the neck and facial areas. A mass was recognized at birth in five children, and the sixth patient was 2 1/2 years old at diagnosis. Four of the six neoplasms contained one or another element of endodermal sinus tumor; two of these had a mixed pattern of endodermal sinus tumor and teratoma. The other two cases were purely teratomas. The serum alpha-fetoprotein was known to be elevated in three children whose tumors had endodermal sinus elements; it returned to normal level in two of the children, but remained high in the one fatal case. Placental alkaline phosphatase and alpha-fetoprotein were demonstrated immunohistochemically in two of the three cases, with available tissue containing endodermal sinus tumor. Teratomatous metastases in ipsilateral cervical lymph nodes were found in one patient with a pure teratoma; that patient is disease-free one year after surgery. Only nine previous examples of endodermal sinus tumor have been reported in the head and neck region, exclusive of the central nervous system. There is one other case in the literature of a congenital cervicothyroidal teratoma with metastatic disease. These six neoplasms illustrate the clinical and pathologic spectrum in this nosologically homogeneous, but morphologically diverse, category of tumors.

Alkaline Phosphatase↗
PubMed2001

Expression of Galpha 13 (Q226L) induces P19 stem cells to primitive endoderm via MEKK1, 2, or 4.

Galpha13 mediates the ability of the morphogen retinoic acid to promote primitive endoderm formation from mouse P19 embryonal carcinoma stem cells, a process that includes the obligate activation of Jun N-terminal kinase. Expression of the constitutively activated (Q226L) GTPase-deficient form of Galpha13 mimics retinoic acid and was used to investigate the signaling upstream of primitive endoderm formation. Jun N-terminal kinase 1 activity, MEK1,2, MKK4, and MEKK1 were constitutively activated in clones stably transfected to express Q226L Galpha13. Dominant negative forms of MEKK1 and MEKK4 were expressed stably in the clones harboring Q226L Galpha13. Expression of dominant negative versions of either MEKK1 or MEKK4 effectively blocks both the activation of Jun N-terminal kinase as well as the formation of primitive endoderm. Depletion of MEKK1, -2, or -4 by antisense oligodeoxynucleotides suppressed signaling from Q226L Galpha13 to JNK1 and primitive endoderm formation. We demonstrate that the signal linkage map from Galpha13 activation to primitive endoderm formation in these stem cells requires activation at three levels of the mitogen-activated protein kinase cascade: MEKK1, -2, or -4 for MAP kinase kinase kinase; MKK4 and/or MEK1 for MAP kinase kinase; and JNK1 for MAP kinase.

3T3 Cells↗
PubMed1997

Endodermal cyst of the third ventricle: case report.

OBJECTIVE AND IMPORTANCE: Endodermal cysts are rare lesions that primarily affect the spinal cord. Only a few reports have been published that describe intracranial endodermal cysts, and, in most of the cases, the cysts were located in the posterior fossa. To our knowledge, there have been no reports of endodermal cysts of the third ventricle. CLINICAL PRESENTATION: A symptomatic endodermal cyst of the third ventricle in a 28-year-old man is presented. The patient demonstrated signs of increased intracranial pressure and reported a progressive loss of vision in his right eye. Neuroradiological imaging revealed obstructive hydrocephalus and a lesion inside the third ventricle measuring 1.2 cm in diameter and occluding the interventricular foramen. INTERVENTION: The cyst was successfully removed via a transcallosal-transforaminal approach. Postoperatively, the patient developed bifrontal effusions for some days. Hydrocephalus was diminished, but his vision had only slightly improved. CONCLUSION: To our knowledge, this is the first published report of an endodermal cyst occurring in the third ventricle, and represents a further example of the broad spectrum of lesions affecting that location.

Adult↗