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Biomedical subjects

A Aharonov

Publications and source records attributed to A Aharonov.

18 recordsLinked to original sources
PubMed1978

Epidermal growth factor induced membrane changes in 3T3 cells.

Epidermal growth factor (EGF) is a mitogen for Swiss 3T3 cells. Short incubation periods with physiological concentrations of EGF induced increased binding of Swiss 3T3 cells to Con A-coated nylon fibers. This effect was not induced in an EGF non-responsive 33 variant, in the transformed murine XC cells or in Swiss SV3T3 cells. The increase in Con A fiber-binding seems to be specific for EGF, since it was not observed in response to insulin, prostaglandin F2alpha or a higher serum concentration, which also initiate cell devision of confluent quiescent 3T3 cells. EGF also reduced Con A-mediated hemadsorption to 3T3, but had no effect on hemadsorption by the EFG non-responsive 3T3 variant. There was no change in the number of Con A-receptors on 3T3 cells after EGF treatment. Binding to WGA-coated fibers and WGA-mediated hemadsorption were not effected by preincubation with EGF.

Clone Cells↗
PubMed1978

Mitogens for murine embryo cell lines.

The growth-promoting activities of fetal bovine serum, cortisol, phorbol myristate acetate, prostaglandin F2alpha, insulin, epidermal growth factor, and fibroblast growth factor were evaluated on four murine embryo cell lines (Swiss 3T3, Balb 3T3, M2, and C3H10T 1/2). Each cell has an unique response spectrum to this collection of reported mitogens. Phorbol myristate acetate and prostaglandin F2alpha were active only on selected cell lines; cortisol was inactive on all four lines. Serum, epidermal growth factor, and fibroblast growth factor were able to stimulate cell division in all four lines, albeit to varying degrees for the different target cells.

Animals↗
PubMed1978

Mitogenic response to epidermal growth factor: relationship to number, affinity, and down-regulation of EGF receptors in three murine embryo cell lines.

Swiss 3T3 and C3H-M2 cells have a greater mitogenic response to epidermal growth factor (EGF) than do C3H10T 1/2 cells. The latter cell line, however, has a number of EGF receptors per cell intermediate between the two cell lines that have a more vigorous response to EGF. Scatchard analysis of binding data indicate that all three cell lines have one class of EGF receptor, with indistinguishable affinity for the ligand. When exposed to 10-nM EGF all three cell lines "down-regulate" their EGF receptors with the same time course, and to the same percentage of initial receptors.

Cell Line↗
PubMed1977

Specific radiolabeling of a cell surface receptor for epidermal growth factor.

A photoreactive derivative of epidermal growth factor (EGF) has been used to identify and specifically label a membrane receptor for EGF on mouse 3T3 cells. Photoactivable EGF, labeled with 125I, was incubated with 3T3 cells and then photolyzed in situ to generate a nitrene capable of reacting with a wide variety of chemical bonds. Analysis of the system by sodium dodecyl sulfate/polyacrylamide gel electrophoresis revealed, besides the band of EGF, only one other major radioactive band, at a position indicating an apparent molecular weight of 190,000. This band was absent when a nonresponsive and nonbinding variant of 3T3 was used. A direct proportionality between binding activity and crosslinked complex formation was demonstrated using a variety of binding conditions. "Down regulated" cells, in which EGF binding activity was greatly reduced by prolonged incubation with an appropriate concentration of EGF, also had a decrease in covalent complex formation proportional to the decrease in EGF binding activity.

Affinity Labels↗
PubMed1977

Cytophilic antibodies in experimental autoimmune myasthenia gravis.

Macrophage-cytophilic antibodies, with acetylcholine receptor specificity, are present in rabbits with experimental autoimmune myasthenia gravis (EAMG). Such antibodies may have a significant role in the immunologic mechanism involved in the pathogenesis of myasthenia gravis. The induction of EAMG in rabbits was performed by injection of purified AChR from the electric organ of Torpedo californica. Both the binding of AChR specific cytophilic antibodies to normal macrophages and the presence of such antibodies bound in vivo to macrophages of sick animals were demonstrated in vitro. The amount of cytophilic antibodies was determined by measuring cell-associated radioactivity after the addition of 125I-AChR. Cytophilic antibodies capable of binding to normal alveolar macrophages were detected in all animals 14 days after immunization, and were maintained through the severe stages of the disease. In addition, cytophilic anti-AChR antibodies were shown to be bound in vivo to alveolar macrophages drawn from severely sick rabbits, as was measured by a direct 125I-AChR binding to such macrophages. The role of cytophilic antibodies and in particular of macrophage-associated cytophilic antibodies in the pathogenesis of autoimmune diseases is not clear yet. The availability of AChR specific cytophilic antibodies can now be utilized for studying their role in the immunopathogenesis of EAMG.

Acetylcholine↗
PubMed1976

Immunosuppression of experimental autoimmune myasthenia gravis by hydrocortisone and azathioprine.

Experimental autoimmune myasthenia gravis (EAMG), induced in rabbits by injection of acetylcholine receptor (AChR) from Torpedo californica, was suppressed by appropriate treatment with hydrocortisone or with azathioprine. Administration of hydrocortisone in gradually increasing doses, starting at the time of immunization with the receptor, prevented exacerbation of the disease in the early stages of treatment, as was the case when hydrocortisone was administered in high doses from the beginning. Prolonged administration of the antimetabolite azathioprine (Imuran) prevented the appearance of EAMG, for at least 4 months, in rabbits immunized with AChR. Cell-mediated immunity to AChR was demonstrated to be significantly decreased in such treated animals. The effects of hydrocortisone and azathioprine on EAMG support the view that the disease involves an immunologically cell-mediated mechanism and indicate that the experimental disease can serve as a useful model for chemotherapy of the human disease.

Acetylcholine↗
PubMed1975

Passive transfer of experimental autoimmune myasthenia by lymph node cells in inbred guinea pigs.

Passive transfer of experimental autoimmune myasthenia (EAM) was performed with lymph node cells from donor guinea pigs immunized with purified acetylcholine receptor (AChR) from Torpedo californica. Recipient animals revealed the same clinical signs and electromyographic patterns as observed in actively challenged animals. These phenomena are parallel to the clinical manifestations of the human disease myasthenia gravis, in which cellular response to AChR was recently demonstrated.

Acetylcholine↗
PubMed1975

Humoral antibodies to acetylcholine receptor in patients with myasthenia gravis.

Sera from patients with myasthenia gravis (M.G.) were studied by the quantitative micro-scale complement-fixation assay for the presence of humoral antibodies against acetylcholine receptor (AChR). The purified receptor was extracted from the electrogenic tissue of the electric ray, Torpedo californica. A significant difference in the antibody titres was observed between myasthenic and non-myasthenic patients. Out of fifteen patients with myasthenia gravis, at least 12 (80%) had antibodies against AChR. Only one case out of twenty-four controls had an indication of anti-receptor antibodies. In view of observations on the role of AChR as the autoantigen in myasthenia gravis, such antibodies may have significance in producing the neuro-muscular block characteristic of the disease.

Acetylcholine↗
PubMed1975

Myasthenia gravis and acetylcholine receptor. Effect of steroids in clinical course and cellular immune response to acetylcholine receptor.

Lymphocytes from patients with myasthenia gravis (MG) were transformed when cultured in vitro with an acetylcholine receptor fraction extracted from the electric organ of an electric eel. Marked diminution of the cellular response to acetylcholine was shown in patients who improved clinically with prednisone treatment. The transient clinical deterioration during the first days of prednisone treatment was accompanied by a transient increase in lymphocyte response. These findings that an in vivo sensitization of lymphocytes to self-acetylcholine receptor may occur in MG, and that a cell-mediated autoimmune mechanism may be important in the pathogenesis of the neuromuscular block. The present observations indicate that prednisone provides a measure of immunosuppression in MG. The transient clinical deterioration during the first days of prednisone therapy may reflect an enhancement of cell reactivity by this drug.

Acetylcholine↗
PubMed1975

Immunological relationship between acetylcholine receptor and thymus: a possible significance in myasthenia gravis.

A defined immunological cross-reaction was observed between acetylcholine receptor fraction from the electric eel, Electrophorus electricus, and two calf thymus fractions. The cross-reaction was demonstrated on the cellular level by means of the lymphocyte transformation technique, and on the humoral level, by means of the microcomplement fixation assay. In the human disease myasthenia gravis both acetylcholine receptor at the neuromuscular junction and the thymus are affected, probably by an autoimmune mechanism. The immunological cross-reaction between acetylcholine receptor and thymic components may explain the association between endplate and thymus disorders in myasthenia gravis.

Acetylcholine↗
PubMed1975

Cellular immune response to acetylcholine receptor-rich fraction, in patients with myasthenia gravis.

Lymphocytes from patients with myasthenia gravis were stimulated when cultured in vitro with an electric eel extract enriched in acetylcholine receptor. No stimulation was observed with other antigens from nerve or muscle origin. Lymphocytes from non-myasthenic patients showed no response to any of these antigens. These findings suggest that an in vivo sensitization of lymphocytes to self acetylcholine receptor may occur in myasthenia gravis. The presence of sensitized lymphocytes, probably resulting from an autoimmune mechanism, might be an important factor in the pathogenesis of the neuromuscular block in this disease.

Acetylcholine↗