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M C Van Peteghem

Publications and source records attributed to M C Van Peteghem.

10 recordsLinked to original sources
PubMed1984

Effect of microtubule inhibitors on the expansion of hypoblast and margin of overgrowth of chick blastoderms.

The effect of the microtubule inhibitors, Nocodazole and taxol, was studied on the expansion of fragments of chick hypoblast (8 to 10 h incubation) and of margin of overgrowth (24 h incubation) cultured on artificial substrata and on the epiboly in intact blastoderms (24 h incubation). Immunocytochemical staining of these cells with antiserum against tubulin showed that 1 micrograms Nocodazole/ml caused disassembly of microtubules, and that 1 microgram taxol/ml led to increased but unordered assembly. The solvent dimethylsulphoxide had no effect. At these concentrations both microtubule inhibitors led to rapid arrest of the expansion of fragments of hypoblast and of margin of overgrowth in culture, and of the epiboly in intact blastoderms. Time-lapse films showed that inhibition of expansion in both situations was reversible within 2 h after removal of the drugs. Phase-contrast microscopy showed remarkably little difference between the morphology of treated as compared to untreated cultures. Measurements of the height of the cells on sectioned fragments of margin of overgrowth showed no differences between treated and untreated cultures. These results suggest that the cytoplasmic microtubule complex is important both for epiboly and for the migration of hypoblast cells in the chick blastoderm. The mechanisms of this microtubule-related migration are not understood.

Alkaloids↗
PubMed1983

Interaction of three human malignant cell lines with chick hypoblast in culture.

The hypoblast (lower layer) was dissected from young chick blastoderms and explanted in vitro, where it formed an epitheloid sheet. Cells from the following malignant lines were explanted on top of the sheet both as aggregates and as cell suspensions: Hu456 human bladder carcinoma, SAOS-2 human osteosarcoma, LICR(LOND)-HN-4 laryngeal carcinoma. The interaction of the malignant cells with the hypoblast was studied by time lapse cinephotography, light microscopy, and transmission electron microscopy. All malignant cells penetrated through the hypoblast, so that a gradually enlarging hole formed in it. Apart from this common pattern of behaviour, the three types of malignant cells differed in their interactions with the hypoblast in the following ways. 1) Both the Hu456 and to a lesser extent the SAOS-2 cells brought about an initial retraction of the hypoblast so that a temporary cell-free space was formed. No such retraction occurred in response to the LICR-(LOND)-HN-4 cells. 2) Each of the three types of malignant cells migrated for some distance beneath the hypoblast, and in this area of underlap, there were differences in the amount and disposition of extracellular material. Thus, there was more extracellular material between the hypoblast and underlying SAOS-2 cells than between the hypoblast and underlying Hu456 cells, whilst there was no extracellular material between the hypoblast and underlying LICR(LOND)-HN-4 cells. Indeed, the hypoblast and LICR(LOND)-HN-4 cells often shared desmosomes. 3) When explanted as aggregates on hypoblast Hu456 and SAOS-2 cells left the corona and migrated as solitary cells underneath the hypoblast in contrast with control aggregates explanted on plastic. These cells which had migrated beneath the hypoblast were flatter than their corresponding control cells which had spread on the plastic substrate. The flatter cells appeared to have been using the extracellular materials as a substrate, rather than the plastic. Such differences in the migratory behaviour between experimental and control cultures were not observed with LICR(LOND)-HN-4 cells.

Animals↗
PubMed1982

Interaction of malignant MO4 cells with chick hypoblast in culture.

Malignant MO4 mouse fibrosarcoma cells were confronted with fragments of hypoblast from stage 4 (Vakaet 1970) blastoderms in different dispositions either permitting or preventing contact of the hypoblast with the tissue culture plastic. Explantation of an MO4 cell aggregate on top of 24 h-old-hypoblast caused retraction of the hypoblast. Contact inhibition of ruffling in hypoblast cells at the inner margin, by MO4 cells migrating radially from the aggregate, prevented closure of the hole brought about by the initial retraction. Disintegration of hypoblast was not observed. Migration of MO4 cells during the first 24 h was faster from an aggregate explanted on top of hypoblast than from an aggregate explanted on tissue culture plastic. Hypoblast fragments explanted on top of confluent layers of MO4 cells attached and spread during the first 12 h. Later, the hypoblast progressively disintegrated. Here, MO4 cells accumulated underneath the hypoblast. We concluded 1) that the hypoblast attracted the MO4 cells by influencing their pattern of migration and 2) that contact with the artificial substrate allowed survival of hypoblast confronting malignant MO4 cells. Ultrastructural analysis suggested that formation of extracellular material played a major role in the interaction between the normal tissue and the malignant cells.

Animals↗
PubMed1980

Phagocytic capacity of invasive malignant cells in three-dimensional culture.

To study the phagocytic capacity of invasive malignant cells, fragments of the hypoblast from chick blastoderms were confronted in three-dimensional culture with spheroidal aggregates of 1) malignant virally transformed C3H mouse cells (MO4), 2) HeLa cells and 3) embryonic chick heart cells. The hypoblast was used because it contains yolk, a marker that is absent in the confronting cells and that can be identified histologically and ultrastructurally. The confronting tissues were incubated on semi-solid agar-agar medium or in fluid medium on a gyrotory shaker. Cultures were followed for 1 to 7 days by stereomicroscopy, cinemicrophotography, light and transmission electron microscopy. Confrontation with MO4 cells of HeLa cells, known to be invasive in vitro, led to complete disappearance of the hypoblast. The fragments of hypoblast were well conserved when cultured alone or confronted with aggregates of chick heart cells. Degeneration of the hypoblast is shown at the area of contact with MO4-cell or HeLa-cell aggregates, in contrast to heart cells. Filopodia-like extensions from the MO4 or HeLa cells penetrate intercellularly, transcellularly and intracellularly into the hypoblast. Phagosomes, containing yolk and unidentified debris are observed in MO4 cells and in HeLa cells, but not in heart cells. These observations demonstrate the phagocytic capacity of invasive malignant cells.

Animals↗
PubMed1979

Comparative studies of two types of "spontaneous" malignant alteration of ST/A mouse lung fibroblasts propagated in vitro.

Two types of apparently spontaneous malignant alterations of fibroblastlike ST/a mouse lung cells (ST-L cells) grown in vitro are described. One type is characterized by a high tumorigenic potential of the altered cells in nonconditioned syngeneic recipients, a fibroblastlike morphology with cell surface showing very few microvilli by scanning electron-microscopy (SEM), and a growth pattern typical of nontransformed cells. These cells were described as R- cells. The other type is characterized bya low tumorigenic potential in non-conditioned, immunocompetent syngeneic recipients, rounding up of the cells which by SEM showed numerous microvilli on the surface, and a growth pattern typical of transformed cells. These cells were described as round cells or R+ cells. In immunoincompetent mice, R+ cells readily produced sarcomas, which grew faster than those produced by R- cells. Both types of ST-L cells expressed murine leukemia virus (MuLV) when tested in a peroxidase anti-p30 plaque test. The concentration of murine leukemia virus envelope glycoprotein (gp70) has previously (5) been shown to be threefold higher in R+ cells compared to R- cells. Furthermore, round-cell transformation was accompanied by the development of crossreacting rejection antigens protective against a secondary shallenge with Ehrlich ascites tumor and with syngeneic dimethylbenzanthracene induced ST/a mouse leukemia (STABAL). A similar protection was obtained by preimmunization with a cloned embryonic feral mouse cell line (SC-1) infected with ST-L virus as well as with virus-free SC-1 cells, suggesting the presence of rejection antigens both of viral (gp70) and nonviral origin.

Animals↗
PubMed1978

Confronting subsurface cisternae and desmosomes in HELA monolayer cultures.

Confronting subsurface cisternae (CSC) and desmosomes are abundant at sites of parallel apposition of plasma membranes in confluent epitheloid monolayers of HeLa cells. Both structures are absent in young and subconfluent cultures, where stable intercellular contacts do not occur. They first appear when the plane of intercellular contact approaches towards the vertical; they disappear when cells separate spontaneously at superconfluency or by treatment with EDTA. The structure of CSC, lacking ribosomes at their side facing the plasma membrane, might fit the production of glycoproteins involved in intercellular adhesion.

Cell Separation↗
PubMed1977

Colloidal iron binding to the surface of HeLa cells, spreading in monolayer culture.

We have used the colloidal iron (CI) binding technique, adapted for transmission electron microscopy, for semiquantitative evaluation of the negative charge density at the surface of HeLa cells in monolayer culture. The surface area increases when HeLa cells spread on the substrate. This increase brings about a decrease in the thickness of the CI rim, indicating a decrease in negative surface charge density. This phenomenon implicates lowering of the electrostatic repulsion, and explains the formation of intercellular contacts at the level of spread parts of the cell. Because of lack of penetration, CI particles are absent in regions of cose apposition between cells and between cells and substrates. Absence of CI binding in broader intercellular or cell-substrate spaces was explained through masking of the anionic groups.

Cell Membrane↗
PubMed1976

Cytochemistry of colloidal iron binding to the surface of Hela cells and human erythrocytes.

It seems from the literature that colloidal iron (C.I.) binding sites on cell surfaces cannot be completely removed by treatment with Vibrio Colerae alpha-neuraminidase. We wondered if C.I. particles bind to negative groups other than the carboxyl groups of sialic acids. Using HeLa cells from suspension cultures and fresh human erythrocytes, we examined, with the transmission electronmicroscope, the influence of the following enzymatic and histochemical treatments on C.I. staining: alpha-neuraminidase; hyaluronidase; ribonuclease; alpha-amylase; mild methylation (MM); MM + saponification (Sap.); MM + Sap +MM; MM + Sap + alpha-neuraminidase; active methylation (AM); AM + Sap; AM + Sap + AM; AM + Sap + alpha-neuraminiadase; CH3OH (80%); Sap. It seemed from these experiments that the carboxyl groups of alpha-neuraminidase sensitive sialic acids constitute the majority of binding sites for C.I. to these particular cells. The most interesting candidates for the residual binding of C.I. are carboxyl groups of alpha-neuraminidase resistant molecules, sulfon, sulfin, and sulfate groups.

Binding Sites↗