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At least 19 recordsLinked to original sources
PubMed1985

A teratocarcinoma-derived endoderm stem cell line (1H5) that can differentiate into extra-embryonic endoderm cell types.

We investigated the ability of the teratocarcinoma-derived, epithelial-type cell line 1H5 to differentiate into either of the two pathways to primary endoderm, and tested the hypothesis that 1H5 represents a state similar to primitive endoderm in the late 4th-day blastocyst. Like other endodermal cell types, 1H5 cells mixed with embryonal-carcinoma cells sort out into "embryoid bodies" or structures that resemble 4th-day mouse embryos. The epithelial line conforms morphologically and biochemically to the few known characteristics typical of primitive endoderm. The present study demonstrates that the formation in vitro of overt visceral endoderm is readily achieved. The spontaneous arrangement of the cells into a cystic form is followed by the appearance of several markers of visceral endoderm, most notably alphafetoprotein, which is detected when 1H5 cells are cultured either in the presence of retinoic acid or when the cells interact with embryonal-carcinoma cells in a specific spatial arrangement after sorting out. However, some less specific properties of visceral endoderm are not expressed. Although 1H5 differentiates histologically into parietal-like endoderm in the tumor form, parietal cells cannot yet be identified with certainty in vitro because of the paucity of parietal-specific markers. The 1H5 cell line could provide a useful system for studying the characteristics and mechanisms underlying visceral-endoderm differentiation in vitro, since it has the distinct advantage that homogeneous cultures are produced, in contrast to other teratocarcinoma cell lines such as F9 which differentiate into a mixture of cell types.

Animals↗
PubMed1992

Ultrastructural analysis of differentiation of rat endoderm in vitro. Adipose vascular-stromal cells induce endoderm differentiation, which in turn induces differentiation of the vascular-stromal cells into chondrocytes.

Isolated definitive endoderm from 9-day-old rat embryos was cultivated up to 24 days in plastic and glass petri dishes and on developing vascular-stromal cells (mesenchymal cells) from epididymal white and interscapular brown adipose tissue of 4-week-old male rats. Explants were analyzed histologically and ultrastructurally. Endoderm attached to the bottom of the glass or petri dishes degenerated under one week of cultivation. Endoderm free floating in the culture medium developed into unilaminar vesicles whose flat epithelium did not differentiate. However, endoderm inoculated on developing mesenchymal cells differentiated into glandular explants or into ciliated pseudostratified columnar respiratory epithelium. The glandular explants were made up of at least four different kinds of cells whose cytoplasm showed predominantly: a) polyribosomes, b) lysosomes, c) mitochondria or d) cytoskeletal filaments. Endodermal cells differentiated only if, during cultivation, they were in contact with or in close proximity to developing mesenchymal cells. Endoderm differentiating into the respiratory epithelium in turn directed differentiation of the underlying vascular-stromal cells into lamina propria cells and chondrocytes. Cultivated vascular-stromal cells in the upper layers became thicker, ellipsoid in shape and with enlarged intercellular space. They appeared to be lamina propria cells and, together with the respiratory epithelium, built folds of respiratory mucosa. The vascular-stromal cells in the layers close to the bottom developed into chondrocytes; i.e., the cells became oval and agglomerated in nest like structures with a defined extracellular matrix. Their cytoplasm contained abundant cisternae of rough endoplasmic reticulum and numerous vacuoles with PAS positive substance. These observations showed that even developing vascular-stromal cells from adipose tissue from postlactating rats can trigger the process of definitive endoderm differentiation. Once triggered, differentiating endoderm influenced differentiation of the vascular-stromal cells into the cells and tissues of a wall of the respiratory tract.

Adipose Tissue↗
PubMed1987

Reversible interconversion between primitive endoderm- and parietal endoderm-like F9 cells demonstrated by mRNAs expression.

The differentiation of retinoic acid-treated F9 cells (primitive endoderm-like F9 cells) into parietal endoderm-like F9 cells induced by dibutyryl cAMP was studied as a culture model of the morphogenesis of early mouse embryo. For this purpose, 6 cDNA clones coding for mRNAs specifically expressed in parietal endoderm-like F9 cells were selected. Northern hybridization of RNA extracted from variously treated F9 cells to nick-translated plasmid DNA of these clones demonstrated the reversible expression of many mRNAs depending on the presence of dibutyryl cAMP in the culture medium. This result suggested that the differentiated state of parietal endoderm, which is formed from primitive endoderm at a position adjacent to the trophectoderm in mouse embryo, can be reversed if the local signal is removed. One of the selected clones, pLAM, hybridized to an mRNA of 6.3 kb and selected mRNA producing a laminin B subunit in an in vitro translation system. This clone has an inserted sequence of 3.1 kb. Among the restriction sites in this sequence, six were consistent with those in a 1.7 kb inserted sequence of pPE 49 and pPE 386, which were isolated by Barlow et al. as laminin B1 clones. An XbaI site found in both pPE 49 and pPE 386 was, however, not found at the corresponding position of pLAM. Dot hybridization of RNA with pLAM showed that expression of laminin B in F9 cells is stimulated more than 100-fold during differentiation of F9 stem cells into parietal endoderm-like F9 cells.

Animals↗
PubMed1979

Endodermal germ cell carcinoma (endodermal sinus tumor) of the vagina in infant girls.

An endodermal sinus tumor (endodermal germ cell carcinoma) was diagnosed in a 1-year-old girl in the vagina after hemorrhage; the tumor was completely removed by radical abdominal surgery. Postoperative polychemotherapy was performed for two years with Actinomycin D, Adriamycin, Vincristin, and Cyclophosphamide. The infant is now tumor-free for 26 months, showing almost normal somatic and psychic development. The characteristic histological patterns and clinical course of this strongly malignant tumor are demonstrated, based on 25 published case reports of endodermal sinus tumors in the vagina of little girls (aged 5-26 months). This neoplasm in early infancy has to be separated from the clear-cell adenocarcinoma of the vagina which occurs after puberty in adolescent girls and young women, and is induced by stilbestrol therapy to the mother during early pregnancy.

Adenocarcinoma↗
PubMed1989

Actin cytoskeleton of extraembryonic endoderm and teratocarcinoma-derived endoderm cells.

Distinct F-actin- and myosin-containing stress fibers were observed in situ in many endoderm cells of parietal yolk sacs from 11-day mouse embryos. In visceral endoderm (VE) such fibers were not seen, and F-actin was concentrated in the cell periphery. Correspondingly, in electron microscopy ventral cell membrane-associated bundles of microfilaments were revealed in the periphery of parietal endoderm (PE) cells but not in VE cells. Both PE and VE cells formed stress fibers in primary cultures. Undifferentiated F9 embryonal carcinoma cells formed only short actin spikes and fibrils irrespective of growth substratum. In PE-like derivatives of F9 cells, on the other hand, distribution of F-actin was markedly affected by the growth substratum: They formed distinct stress fibers when plated on fibronectin but did not when plated on gelatin. Similarly, in teratocarcinoma-derived PE cells (PYS-2) adhesion to fibronectin induced the formation of distinct bundles of F-actin and plaques of vinculin. The results suggest that the susceptibility of teratocarcinoma cell actin cytoskeleton to the influence of molecular composition of surrounding matrix is developmentally regulated. On the other hand, the reason for the presence of stress fibers in PE cells and for their absence in VE cells is unclear.

Actins↗
PubMed1987

Congenital polycystic tumor of the atrioventricular node (endodermal heterotopia, mesothelioma): a histogenetic appraisal with evidence for its endodermal origin.

The small, variously designated, primary atrioventricular node tumor has been considered to be of endothelial, endodermal, or mesothelial origin. To identify its derivation, we studied seven tumors using silver staining and immunocytochemical labeling with a variety of antibodies. Cytoplasmic argyrophil granules but not argentaffin granules were found in isolated cells among the more numerous tubule-lining cells in four tumors. Serotonin and calcitonin were demonstrable in seven and six tumors, respectively, in a similar distribution to that of the argyrophil cells. A positive reaction of different distribution from that of the argyrophil cells was noted in a varying number of tubule-lining cells for carcinoembryonic antigen, epithelial membrane antigen, and blood group antigen in seven, four, and seven tumors, respectively. No activity was noted in the tumor cells for factor VIII-related antigen or a number of peptides. An endodermal rather than mesothelial or epithelial origin for the tumor is substantiated by the presence of neuroendocrine cells in the midst of the more numerous carcinoembryonic-antigen-positive lining cells of the tumor tubules.

Atrioventricular Node↗
PubMed1986

Cell fate and cell lineage in the endoderm of the presomite mouse embryo, studied with an intracellular tracer.

The fate of the embryonic endoderm (generally called visceral embryonic endoderm) of midstreak to neural plate stages of the mouse embryo was studied by microinjecting horseradish peroxidase (HRP) into single axial endoderm cells in situ, and tracing the labeled descendants to early somite stages in vitro. Axial endoderm cells along the anterior fifth of the late streak/neural plate stage embryo contributed descendants either to the yolk sac endoderm or to the anterior intestinal portal. Cells of the exposed head process contributed to the trunk endoderm and notochord; neighboring endoderm cells contributed to the dorsal foregut. Contributions to the ventral foregut came from endoderm at, and anterior to, the distal tip of the younger, midstreak embryo (in which the head process was not yet exposed). Endoderm over the primitive streak contributed to the postsomite endoderm. We argue from these results and those in the literature that during gastrulation the axial embryonic endoderm is of mixed lineage: (1) an anterior population of cells is derived from primitive endoderm and contributes to the yolk sac endoderm; (2) a population at, and anterior to, the distal tip of the midstreak embryo, extending more anteriorly at late streak/neural plate stages, is presumed to emerge from primitive ectoderm at the beginning of gastrulation and contributes to the foregut and anterior intestinal portal; (3) the axial portion of the head process that begins to incorporate into the ventral surface at the late streak stage contributes to notochord and trunk endoderm. Cells or their descendants that were destined to die within 24 hr were evident at the midstreak stage. There was a linear trend in the incidence of cell death among labeled cells at the late streak/neural plate stages, ranging from 27% caudal to the node to 57% in the anterior fifth of the embryo. The surviving axial endoderm cells divided sufficiently fast to double the population in 24 hr.

Animals↗
PubMed1987

Cell fate, morphogenetic movement and population kinetics of embryonic endoderm at the time of germ layer formation in the mouse.

The fate of the embryonic endoderm (generally called visceral embryonic endoderm) of prestreak and early primitive streak stages of the mouse embryo was studied in vitro by microinjecting horseradish peroxidase into single axial endoderm cells of 6.7-day-old embryos and tracing the labelled descendants either through gastrulation (1 day of culture) or to early somite stages (2 days of culture). Descendants of endoderm cells from the anterior half of the axis were found at the extreme cranial end of the embryo after 1 day and in the visceral yolk sac endoderm after 2 days, i.e. they were displaced anteriorly and anterolaterally. Descendants of cells originating over and near the anterior end of the early primitive streak, i.e. posterior to the distal tip of the egg cylinder, were found after 1 day over the entire embryonic axis and after 2 days in the embryonic endoderm at the anterior intestinal portal, in the foregut, along the trunk and postnodally, as well as anteriorly and posteriorly in the visceral yolk sac. Endoderm covering the posterior half of the early primitive streak contributed to postnodal endoderm after 1 day (at the late streak stage) and mainly to posterior visceral yolk sac endoderm after 2 days. Clonal descendants of axial endoderm were located after 2 days either over the embryo or in the yolk sac; the few exceptions spanned the caudal end of the embryo and the posterior yolk sac. The clonal analysis also showed that the endoderm layer along the posterior half of the axis of prestreak- and early-streak-stage embryos is heterogeneous in its germ layer fate. Whereas the germ layer location of descendants from anterior sites did not differ after 1 day from that expected from the initial controls (approx. 90% exclusively in endoderm), only 62% of the successfully injected posterior sites resulted in labelled cells exclusively in endoderm; the remainder contributed partially or entirely to ectoderm and mesoderm. This loss from the endoderm layer was compensated by posterior-derived cells that remained in endoderm having more surviving descendants (8.4 h population doubling time) than did anterior-derived cells (10.5 h population doubling time). There was no indication of cell death at the prestreak and early streak stages; at least 93% of the cells were proliferating and more than half of the total axial population were in, or had completed, a third cell cycle after 22 h culture.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1989

Plasminogen activator expression in F9 teratocarcinoma embryoid bodies and their endoderm derivatives.

Plasminogen activators are believed to play an important role in tissue remodeling and cell migration. During mouse embryogenesis, visceral endoderm secretes urokinase-type plasminogen activator (uPA) whereas parietal endoderm secretes tissue-type plasminogen activator (tPA). Visceral endoderm from F9 embryoid bodies can transdifferentiate into parietal endoderm under the appropriate culture conditions. We have examined at the protein and mRNA levels the type of plasminogen activator expressed in whole embryoid bodies, visceral endoderm and its parietal endoderm derivatives. Our experiments show that the visceral endoderm on F9 embryoid bodies synthesizes and secretes substantial amounts of both tPA and uPA. In contrast, the parietal endoderm derived directly from the visceral endoderm secretes dramatically increased levels of tPA and decreases production of uPA to low or below detectable levels. These data support the finding that visceral endoderm can transdifferentiate to parietal endoderm. In addition, this transition provides an excellent model for studying the molecular basis of the coincident down- and upregulation of the two plasminogen activators as well as their potential function during embryogenesis.

Animals↗
PubMed1987

Cell lineage analysis of the primitive and visceral endoderm of mouse embryos cultured in vitro.

Cell lineages of the primitive endoderm and the visceral endoderm of mouse embryos were examined by culturing whole embryos in vitro. The primitive endoderm and visceral endoderm cells could be labelled by incubation of embryos in a medium containing horse radish peroxidase (HRP). HRP localization was chased throughout the culture period. The results show that the visceral endoderm derives from the primitive endoderm, and the visceral endoderm forms only the extra-embryonic endoderm (yolk sac endoderm) of the conceptus. The definitive endoderm which is probably derived from the head process, newly appears on the ventral surface of the embryo.

Animals↗
PubMed1991

[Morphological and functional features of endodermal cells in rat yolk sac, with special reference to the fetal macrophage differentiation].

Morphological and functional features of the yolk sac endodermal cells with special reference to the fetal macrophage differentiation were investigated morphologically under the light and electron microscopes and immunologically with the antigen phenotypic analysis and the phagocytic activity-test, using the syngeneic DA rat-embryos from 8 to 16 days of gestation. Based on the staining property with toluidin blue and the ultrastructural features, the endodermal layer from day 8 to 16-yolk sacs has been known to consist of two kinds of cell type; 10% "clear" cells with clear cytoplasm and 90% "dark" cells with dark cytoplasm. Numerous primary lysosomes, phagolysosomes, lipid droplets and coated vesicles distributed preferentially in the supranuclear portion of endodermal cells. A broad intercellular space was found between "clear" cells and "dark" cells, indicating the loose intercellular binding. It was often found that "clear" cells tend to migrate from the endodermal layer into the mesenchymal layer, where the poor development of basement membrane was seen between them. Cells phagocytosing red blood cells, that resemble morphologically "clear" cells, were also observed in the fetal liver. At ten hours after latex-injection into the yolk sac cavity of 14 days embryos, some cells which phagocytosed latex beads in their cytoplasm were found in the endodermal layer, and also in the liver tissue and loose connective tissue of fetus. These cells were stained positively with monoclonal antibody Mar3 which recognizes preferentially rat-mononuclear phagocyte system. In vitro-latex uptake of separated endodermal cells was also demonstrated by the culture-study of endodermal cell suspension. The present findings indicate that the yolk sac-endodermal layer derived from the proximal endoderm consists of at least two kinds of cell-population with a great similarity to tissue macrophages in morphological and functional senses, and support the concept that some cell-populations of endodermal layer may migrate into fetal tissue and are closely related to the differentiation of fetal macrophages and their precursors.

Animals↗
PubMed1986

Evidence for the existence of an early common biochemical pathway in the differentiation of F9 cells into visceral or parietal endoderm: modulation by cyclic AMP.

The addition of dibutyryl cyclic AMP (dbcAMP) to aggregate cultures of F9 cells in medium containing retinoic acid (RA) directs the pathway of differentiation into parietal endoderm instead of visceral endoderm. We examined the levels of some of the markers that characterize the two pathways and studied the time of commitment of cells to either direction of differentiation by using immunoprecipitation and enzyme-linked immunosorbent assays (ELISA). For either pathway, the levels and patterns of laminin, type IV collagen, and fibronectin are the same on the first day of differentiation, characterized by slightly decreased levels of laminin and type IV collagen synthesis and an increased level of fibronectin synthesis. These levels reverse on the second day of culture when the pathways diverge markedly. The differentiation pathway, however, can be redirected into the alternate one; parietal endoderm cells become committed after 3 days, whereas visceral endoderm cells are able to change into parietal endoderm cells at any time. Thus, alpha-fetoprotein (AFP)-producing F9 embryoid bodies switched to dbcAMP-containing medium lose the capacity to synthesize AFP and start to express genes characteristic of parietal endoderm. Our results indicate that at least some visceral endoderm cells may redifferentiate into parietal endoderm cells. These phenomena thus mimic features of endoderm differentiation in the mouse embryo.

1-Methyl-3-isobutylxanthine↗
PubMed1986

The outgrowth of parietal endoderm from mouse teratocarcinoma stem-cell embryoid bodies.

Teratocarcinoma stem cells can be used to study certain events occurring during early mouse embryogenesis. We report that the outgrowth of parietal endoderm from teratocarcinoma stem-cell embryoid bodies in vitro is analogous to the same process in vivo in terms of the spatial distribution of endoderm types: only parietal endoderm migrates away from the aggregate, whereas visceral endoderm remains associated with the embryoid body. The outgrowths generated on a substrate of type-I collagen from PSA-1 and retinoic-acid-treated F 9 embryoid bodies were found to be comparable, even though these aggregates express different endoderm types. We demonstrated that retinoic-acid-treated F 9 embryoid bodies that contain essentially only visceral endoderm in suspension culture can nonetheless generate parietal-endoderm outgrowth when plated on type-I collagen, suggesting that substrate interaction plays an important role in inducing parietal-endoderm differentiation. These data indicate the usefulness and relevance of studying endoderm differentiation and outgrowth in vitro employing the teratocarcinoma model system.

Animals↗
PubMed1985

Regeneration of endoderm from primitive ectoderm in the mouse embryo: fact or artifact?

The capacity of immunosurgically (IS) treated inner cell masses (ICMs) versus microsurgically (MS) isolated primitive ectoderms from blastocysts recovered on the 5th day of gestation to regenerate an external layer of endoderm cells in vitro was investigated. While the majority of IS-treated ICMs regenerated such a layer, MS-isolated ectoderms seldom did so. Examination of the two types of tissue fragments revealed that IS-treated ICMs almost invariably retained viable endoderm cells whereas MS-isolated ectoderms did so only exceptionally. The endoderm was found to be more than one cell layer thick in ICMs from 5th day blastocysts, suggesting that some endoderm cells survive IS because they are protected from exposure to antiserum. Typing of the endoderm layer that regenerated following IS treatment of recombinant ICMs composed of genetically dissimilar endoderm and ectoderm provided direct evidence that it originated from residual endoderm cells rather than the underlying ectoderm. Finally, blastocyst injection experiments confirmed that IS-treated ICMs behave like a mixture of ectoderm and endoderm tissue in vivo, and provided no support for the view that cells of the original and regenerated endoderm differ in developmental potential. These findings challenge earlier conclusions concerning cell lineage and determination in the primitive ectoderm that were based on development in vitro of IS-treated ICMs from giant blastocysts.

Animals↗
PubMed1979

The development of hepatogenic potency in the endoderm of quail embryos.

Hepatogenic potency of the endoderm is detectable in the anterior half of the endoderm of quail embryos older than 2-somite stage when endodermal fragments are cultured with or without heterologous chick mesenchymes, in the coelomic cavity of 3-day chick embryos. On the other hand, the posterior half of the endoderm never has hepatogenic potency. The hepatogenic potency of the endoderm is gradually stabilised with increasing age. However, expression of hepatogenesis can be affected when the endoderm is associated with inductively active digestive tract mesenchymes. Mesenchyme taken from the presumptive cardiac region ('cardiac' mesenchyme) of chick embryos is necessary for the uncommitted anterior endoderm to acquire hepatogenic potency, and this effect is specific for the 'cardiac' mesenchyme. The 'cardiac' mesenchyme, however, fails to induce hepatic epithelium in the allantoic endoderm, which can differentiate heterotypically when cultured in combination with digestive tract mesenchymes. The evidence presented in this study suggests that the effect of 'cardiac' mesenchyme on the acquisition of hepatogenic potency in the endoderm is limited.

Animals↗
PubMed1985

Cell surface markers to monitor the process of visceral endoderm differentiation from embryonal carcinoma cells: identification of the stage sensitive to high concentration of retinoic acid.

Two cell surface antigens, brushin and FT-1 were effective in analysis of the process of visceral endoderm differentiation. Brushin was detected on both primitive and visceral endoderm, while FT-1 was detected only on visceral endoderm. When aggregates of N4-1 embryonal carcinoma cells were exposed to 10(-8) M-retinoic acid for more than 2 days, external cells differentiated to multilayered and vacuolized visceral endoderm. However, aggregates treated with 10(-6) M-retinoic acid developed an endoderm layer, which remained one cell thick and was not vacuolized. Cell surface properties of the endoderm cells indicated that the high concentration of retinoic acid inhibited the differentiation pathway at the stage between primitive endoderm cells and visceral endoderm cells. By pulsed exposure to 10(-6) M-retinoic acid, the period sensitive to the high concentration of retinoic acid was shown to be around day 4 after the initial exposure to retinoic acid.

Animals↗
PubMed1989

Immunohistochemical differentiation of clear-cell carcinoma of the female genital tract and endodermal sinus tumor with the use of alpha-fetoprotein and Leu-M1.

The morphologic differentiation between clear-cell carcinoma and endodermal sinus tumors is difficult at times. To improve the accuracy of the diagnosis, the authors studied nine ovarian and eight vaginal clear-cell carcinomas and seven endodermal sinus tumors of the ovary by immunohistochemical methods with the use of antibodies to alpha-fetoprotein and Leu-M1. Sixteen (94.1%) of the 17 clear-cell carcinomas and two (28.5%) of the seven endodermal sinus tumors reacted for Leu-M1, whereas six (85.7%) of the seven endodermal sinus tumors and three (17.6%) of the 17 clear-cell carcinomas stained for alpha-fetoprotein. Three clear-cell carcinomas and two endodermal sinus tumors showed immunoreactivity for both markers. No reactivity for either of these markers was present in one endodermal sinus tumor and one clear-cell carcinoma. All 13 tumors that stained only for Leu-M1 proved to be clear-cell carcinomas, and the four that reacted exclusively for alpha-fetoprotein were endodermal sinus tumors. Therefore, the authors concluded that positive immunostaining for Leu-M1 and negative immunostaining for alpha-fetoprotein support the differential diagnosis of clear-cell carcinoma, whereas a positive reaction for alpha-fetoprotein and a negative reaction for Leu-M1 favor a diagnosis of endodermal sinus tumor. However, positive or negative staining for both markers appears to have no diagnostic value.

Adenocarcinoma↗
PubMed1988

Vitronectin production by human yolk sac carcinoma cells resembling parietal endoderm.

Normal mesenchymal cells, normal epithelial cells and many transformed epithelial cells require serum attachment factors and extracellular matrix proteins for growth and differentiation in vitro, and recent evidence strongly supports a role for extracellular matrix molecules in the regulation of cell movement in vivo during early embryogenesis. We previously described the isolation and characterization of cell lines representative of three types of stem cells most commonly found in human adult testicular teratomas, namely embryonal carcinoma cells, yolk sac carcinoma cells resembling visceral endoderm and yolk sac carcinoma cells resembling parietal endoderm (endodermal sinus tumour cells). Of these three cell types, only endodermal sinus tumour cells, which show particularly malignant behaviour in vivo, have no serum requirement for attachment and growth in vitro. Supernatants from endodermal sinus tumour cells support the attachment of embryonal carcinoma cells in serum-free medium. We demonstrate here that endodermal sinus tumour cells, but not other cell types isolated from testicular teratomas, secrete the serum attachment protein, vitronectin (also known as serum-spreading factor, S-protein or epibolin), as well as fibronectin, laminin and type IV collagen, into serum-free medium. Purified vitronectin from medium conditioned by endodermal sinus tumour cells supported both attachment and spreading of embryonal carcinoma cells in vitro, whereas cells attached but did not spread properly on surfaces coated with fibronectin or laminin. Peptides containing the RGD cell recognition sequence common to many attachment proteins blocked attachment of endodermal sinus tumour cells to untreated tissue-culture plastic in serum-free medium. The results suggest a possible role for vitronectin in regulating cell motility and growth in early development, and in the invasion and spread of teratomas in vivo.

Collagen↗