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Biomedical subjects

C Chany

Publications and source records attributed to C Chany.

At least 91 records · Page 5Linked to original sources
PubMed1979

Lectin-like activity of components extracted from human glomerular basement membrane.

Different fractions of human glomerular basement membranes have been isolated by enzymatic and chemical methods. These fractions were analyzed for their chemical structure and biological activity. The hypothesis that human glomerular basement membrane glycopeptide fractions related to collagenous sequences could act as a lectin-like substance was explored; in fact, extracellular glycoprotein factors play a role in cell-cell interactions and cell adhesion. These collagenous glycopeptides agglutinate human transformed or embryonic cells within 2 hr. The cell agglutination is inhibited by the following sugars: N-acetylglucosamine, N-acetylgalactosamine, and N-acetylneuraminic acid. In addition, the rapid cytoagglutination is followed by a cell spreading effect after a further 20-hr incubation. These data led to the postulate that the maintenance of tissue differentiation is governed by the interaction of cells with peculiar sites of the basement membrane consisting of a proteolysis-resistant association between collagen and matrix glycoprotein.

Agglutination Tests↗
PubMed1979

Human leukocyte interferon: relationship between molecular structure and species specificity.

Human leukocyte interferon can be separated into two classes of subspecies by polynucleotide-agarose affinity chromatography; 30-40% of the molecular species have the polynucleotide-binding property and 60-70% lack affinity for the polynucleotide ligand. When analyzed on sodium dodecyl sulfate/polyacrylamide gel electrophoresis, the former class of interferon has a slower mobility corresponding to the migration of a polypeptide of 21,000 daltons, while the latter class has a faster mobility corresponding to a polypeptide of 13,500-15,000 daltons. By analogy to the behavior of other interferons and a class of nucleotidyl transferases on the polynucleotide-agarose chromatography, we suggest that the human leukocyte interferon having the polynucleotide-binding site is in a possibly "native" conformation and the loss of affinity for polynucleotide results from a degradative alteration of the native molecules. Moreover, the alteration of interferon is accompanied by an increase in heterospecific activity on bovine cells. It is suggested that the polypeptide domain responsible for species specificity may be closely related to the polynucleotide binding area. The modified interferon molecule, however, still conserves its antiviral activity. The simplicity and the high capacity of polynucleotide-agarose chromatography make this a powerful technique for the purification of interferon. The easy separation of these two classes of human leukocyte interferon makes the purification procedures more rational and will facilitate the preparation of both subspecies to a high degree of molecular homogeneity.

Animals↗
PubMed1979

Adverse effects of interferon treatment on the life span of NZB mice.

NZB mice treated with interferon from birth and for over a year, display early some characteristics of the autoimmune disease. In these animals, mortality is clearly higher than in controls. Their death occurs 3 to 6 months before that of mice injected with a "mock" preparation.

Animals↗
PubMed1979

Enhancement of interferon antitumor action by sodium butyrate.

Sodium butyrate together with interferon enhances the antitumor effect of interferon in vivo. When Sarcoma 180 TG cells are inoculated in mice, the mean survival time and final survival rate are greatly increased compared to those for treatment with interferon alone. Similarly, a significant delay in the mean survival time is observed when mice inoculated with L1210 cells are treated with sodium butyrate and interferon. This effect could be due at least in part to a potentiation of interferon action on the tumor cells.

Animals↗
PubMed1978

[Inhibitory effect of the tissue antagonism of interferon on the development of 180/TG Crocker tumor: recognition of a new murine lectin].

Crude and purified murine lectin preparations are extracted from costal cartilage (TAI). They inhibit the antiviral state induced by interferon. They also agglutinate the Crocker 180/TG tumor cells. After IP inoculation in mice, the purified lectin preparation significantly decreases tumor incidence and increases the animal's life span.

Agglutination Tests↗
PubMed1978

Isolation, preliminary characterization, and interferon antagonistic effect of a mammalian lectin-like substance.

We have isolated from mouse costal cartilage a tissue antagonist of interferon (TAI) which accelerates the decay of an established antiviral state. The effect is reminiscent of substances previously isolated from the basement membrane of human amnion. Since we have recently shown that phytohemagglutinin can mimic the biological effect of TAI, we have explored the possibility that TAI could be an animal lectin-like material. First, TAI agglutinates mouse cells; second, this cell agglutination is inhibited by some sugars. Preliminary characterization indicates that the active molecule is a protein. After Sephadex G-100 gel filtration, TAI is found in a peak of 150,000 molecular weight. When purified by isoelectric focusing, this peak shows maximal activities corresponding to an isoelectric point of pH 8.8 TAI binds to polysaccharide residues of the cell membrane which could be its primary site of action, comparable to phytohemagglutinin.

Agglutinins↗
PubMed1978

Effect of ammonium salts on the interferon-induced antiviral state in mouse L cells.

The addition of ammonium salts to cells treated with interferon prevents the development of the antiviral state and destroys it when already established. This treatment does not seem to act on the binding of interferon to the cells but blocks a further step of activation on the cell membrane. The anti-interferon effect of ammonium salts is reversible with a complete recovery of the antiviral state. It is postulated that these salts may stabilize the interferon-receptor complex and thus prevent the changes in configuration necessary for the establishment and maintenance of its biological functions.

Ammonium Chloride↗
PubMed1978

Isoprinosine increases the antitumor action of interferon.

The association of relatively low doses of interferon with an immunostimulant (isoprinosine) enhances the antitumor effect of interferon. After combined treatment, the mean survival time, tumor incidence, and final survival rate are significantly increased in mice inoculated with 10(6) Crocker tumor 180/TG cells when compared to mice treated with interferon alone.

Animals↗
PubMed1977

[Tissue antagonist of interferon : murine substance similar to plant lectins].

A tissue antagonist of interferon (TAI) extracted from mouse costal cartilage contains a substance which has many properties characteristic of plant lectins. After binding to the cell membrane receptors, it agglutines normal and transformed murine cells. In interferon treated cells, it restores virus sensitivity probably through a modification in the distribution of membrane bound cellular antigens.

Agglutination Tests↗
PubMed1977

[Degradation by phytohemagglutinin of the antiviral state induced by interferon].

Phytohaemagglutinin (PHA M and P forms), when added to L 929 cells previously treated by murine interferon, degrades the antiviral state and restores virus sensitivity in the cells. This degradation depends on the amount of the lectin, the contact period with the cell and the presence of PHA membrane receptors. The importance of membrane configuration not only in the induction but also in the maintenance of the antiviral state is discussed.

Cell Membrane↗
PubMed1977

[Potentiating effect of cycloheximide on viral interference].

The degradation of the antiviral state can be delayed in vitro by antimetabolites, when added between 5-7 hours after interferon. We explore in this chronological order whether antiviral resistance induced by Newcastle disease virus (N.D.V.) in vivo could be modified by an antimetabolite. Cycloheximide was selected for this study because of its reversible biological effect and lack of toxicity in our experimental conditions. The model system employed was Syrian Hamsters, using N.D.V. as an interferon inducer and encephalomyocarditis virus (E.M.C.) as a challenge virus. A constant and significant increase in survival of animals treated with N.D.V.+cycloheximide is probably related to a delay in the degradation of the antiviral state and not to interferon superinduction.

Animals↗
PubMed1977

Enhancement of antiviral protection against encephalomyocarditis virus by a combination of isoprinosine and interferon.

The antiviral effect of interferon against encephalomyocarditis (EMC) virus infection in mice was enhanced by isoprinosine. However, the enhancement was only obtained when both interferon and the virus were inoculated into the peritoneum; the inoculation route of isoprinosone did not modify significantly the final results. In addition, the time sequence of injections was of great importance; generally the injection of isoprinosine had to precede that of interferon by a few hours.

Animals↗
PubMed1977

Mechanism of polykaryocyte induction by vesicular stomatitis virus in rat XC cells.

Vesicular stomatitis virus (VSV) induces polykaryocytes in rat embryonic fibroblasts transformed by the Prague strain of Rous sarcoma virus (XC cells). The cell fusion requires the uncoating of the virus in the cell, the synthesis of normally structured G and M proteins and their incorporation into the cell membrane. The synthesis of fully infectious virus is unnecessary. In addition to these antigens, a special yet undefined constitution of the host membrane is also important. With thermosensitive mutants non-defective for G and M antigens, cell fusion is much more extensive at the non-permissive temperature (39-6 degrees C) than at the permissive one (31 degrees C). The importance of these two antigens is also shown using rifampicin-sensitive mutants. We postulate that these two antigens induce in the cell membrane an imbalance in the distribution of phospholipids which then diffuse through membrane junctions to surrounding cells, provoking thereafter the cell fusion.

Animals↗
PubMed1977

Role of the membrane-bound receptor system in the biological activity of interferon.

The model of the interferon receptor system initially proposed in 1973 is now supported by many independent observations and can be described with somewhat more precision. The cell membrane-bound receptor system consists of a nonspecific binding site made up of gangliosides (such as GM2). The activator site is probably formed by glycoproteins. It is likely that interferon has to interact with both sites at the surface of the cell membrane. The activator site carries probably the interferon species specific properties of the receptor, while all the other metabolic steps necessary for the development of antiviral activity are not species specific. The cooperation (resulting most likely in small aggregates) will change the conformational state of the membrane in a way compatible with the action of interferon. We postulate that many other cellular effects of interferon, such as priming, modification of antigenic properties, changes in membrane permeability, increase or decrease in sensitivity to toxins, repression of cellular DNA synthesis could be secondary effects related to cell membrane modulation. Experiments are now in progress to prove or disprove these postulates.

Animals↗
PubMed1976

Permissiveness of mouse, monkey and hybrid cells to encephalomyocarditis (EMC) virus.

Encephalomyocarditis (EMC) virus replicates to high titre in permissive mouse kidney (MKS) cells but poorly in monkey kidney (CV1) cells. The permissiveness of monkey-mouse hybrid cells varies according to their chromosomal content. In monkey cells, the synthesis of both single-stranded and double-stranded virus RNA is restricted; in semi-permissive hybrid clones, the double-stranded RNA is synthesized normally, whereas the synthesis of the single-stranded RNA is inhibited. Thus, it seems that more than one restrictive event is responsible for the low permissiveness of monkey cells to EMC virus.

Animals↗
PubMed1976

Membrane-bound interferon specific cell receptor system: role in the establishment and amplification of the antiviral state.

The cell membrane, in addition to other functions, plays an important role in regulating cell metabolism governed by messenger proteins (or other substances) acting from the outside. The interferon receptor system located in the cell membrane (used as a model) might consist of two components: a binding site and an activator site. As shown by experiments based on competition between interferons for the same receptor, binding is not necessarily followed by activation of the antiviral state. It is possible that polysaccharid residues present in gangliosides play an important role in binding. A critical concentration of interferon molecules in contact with the receptors is needed to induce the antiviral state, which is thus a cooperative process. The activation and probably the amplification of the response require free membrane-bound energy and the integrity of the cytoskeletal components of the cell. Modifications in cell membrane structure can change the response to interferon; on the other hand, interferon might induce changes in the cell membrane which finally result in an altered response to toxins and, in some instances, in recovery of lost contact inhibition in transformed cells.

Adenosine Triphosphatases↗