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Biomedical subjects

M Bar-Eli

Publications and source records attributed to M Bar-Eli.

At least 91 records · Page 5Linked to original sources
PubMed1985

Expression of ki-ras oncogene in tumor cell variants exhibiting different metastatic capabilities.

The expression of oncogenes in well-characterized B16 melanoma and UV-2237 fibrosarcoma cell variants that exhibit distinct metastatic properties was explored. The search for the expression of 11 different oncogenes revealed that the major oncogene in those two tumor systems is the Kirsten-ras (ki-ras). The results indicate that the amounts of specific ki-ras mRNA and the p21 protein are similar in both low- and high-metastatic counterparts. These results suggest that in these systems there is no apparent direct correlation between the amount and expression of the major cellular oncogene so far identified and the metastatic potential of these tumor cells.

Animals↗
PubMed1984

Antibodies to two defined regions of the transforming protein pp60src interact specifically with the epidermal growth factor receptor kinase system.

Antibodies generated against two synthetic peptides corresponding to two defined regions on the transforming protein of Rous sarcoma virus, pp60src, interact specifically with the epidermal growth factor (EGF)-receptor kinase. An antibody directed against a synthetic peptide corresponding to the major phosphorylation site of pp60src interacts specifically with EGF receptor and immunoprecipitates a functional EGF-receptor kinase. The second antibody, which binds close to a region on the src molecule that is required for its kinase activity, also binds to EGF-receptor kinase and prevents the autophosphorylation of the receptor molecules. Neither antibody binds to intact cells, but they do recognize various forms of the solubilized receptor. It is concluded that at least two cytoplasmic domains of the EGF receptor are antigenically and presumably also structurally related to specific domains on pp60src.

Amino Acid Sequence↗
PubMed1983

Expression of a methotrexate-resistant dihydrofolate reductase gene by transformed hematopoietic cells of mice.

DNA-mediated gene transfer was used to introduce DNA from a methotrexate-resistant mouse fibroblast cell line into mouse bone marrow cells. This cell line contained a methotrexate-resistant dihydrofolate reductase, active at 10(-4) M methotrexate, which was electrophoretically separable from the wild-type mouse enzyme. Transformed hematopoietic cells were returned to irradiated mice and selected in vivo by methotrexate administration. Some recipients of transformed marrow cells expressed the electrophoretically distinct, methotrexate-resistant dihydrofolate reductase in hematopoietic cells. These observations suggest that successful transformation of marrow stem cells to methotrexate resistance is accomplished by insertion of a dihydrofolate reductase gene coding for a mutant enzyme that is highly resistant to methotrexate.

Animals↗
PubMed1982

Insertion of new genetic information into bone marrow cells of mice: comparison of two selectable genes.

A system for insertion of new genetic information into mouse hematopoietic cells is described. Two selectable genes were examined: herpesvirus thymidine kinase and a mutant mouse dihydrofolate reductase. The DHFR system appears to be superior in terms of the frequency and stability of gene insertion and expression in hematopoietic tissues. About 70% of mice had indirect (karyotypic) evidence of gene insertion; of these, about 60% (three of five) had stable expression of the inserted mutant DHFR. In contrast, only 13% of mice demonstrated stable karyotypic transformation by HSVtk, and of those with stable transformation five of seven showed persistent viral gene sequences in hematopoietic tissues.

Animals↗
PubMed1981

A neutrophil lysozyme leak in patients with familial Mediterranean fever.

Polymorphonuclear cells derived from the peripheral blood of patients with Familial Mediterranean Fever release more lysozyme in response to high temperature (42 degrees, 46 degrees C) than do control cells. No differences between the FMF and control cells were observed in the release of acid phosphatase, beta-glucuronidase, or lactoferrin. Colchicine treatment had no effect on the measurable release of the enzyme from PMNs derived from FMF patients. The increased release of lysozyme in response to high temperatures appears to be specific to FMF neutrophils, and was not found in PMNs from non-FMF patients with febrile or inflammatory diseases, nor was it seen in monocytes derived from the FMF patients. It is suggested that the increased release of lysozyme from the neutrophils may be of importance in the pathogenesis of FMF.

Acid Phosphatase↗
PubMed1981

Phorbol ester effect on differentiation of human myeloid leukemia cell lines blocked at different stages of maturation.

The control of differentiation by tumor-promoting phorbol diesters including 12-O-tetradecanoylphorbol-13-acetate (TPA) was investigated using cells from human myeloid leukemia lines and sublines that were blocked at different stages of maturation. The myeloid leukemia cells that were blocked at the myeloblast-promyelocyte stage of maturation (KG-1, HL-60, and ML-3) had a prominent response when cultured with TPA. The cells became adherent, developed pseudopodia, displayed macrophage characteristics by light microscopy, developed nonspecific acid esterase activity, phagocytized yeast, slightly reduced nitro blue tetrazolium, displayed Fc-immunoglobulin G receptors, and killed bacteria. Lysozyme secretion and enzyme activity for beta-glucuronidase and acid phosphatase increased 2- to 20-fold concomitant with macrophage differentiation. The myeloid leukemia cells that were blocked at the undifferentiated myeloid blast stage of maturation (KG-1a and K562) were completely resistant to TPA-induced macrophage differentiation. We examined ten macrophage functions in the myeloid cell lines and sublines after exposure to phorbol diesters. The leukemic lines blocked at the myeloblast-promyelocyte stage of maturation expressed almost all the macrophage-specific functions. Phorbol diesters probably induced differentiation through a common cellular mechanism because the macrophage-differentiated events could not be dissociated. In sharp contrast, the early myeloid blast cells (KG-1a and K562) were incapable of acquiring any of the macrophage-specific functions after exposure to phorbol diesters. The KG-1a variant, in particular, should provide a good model to help elucidate the regulatory mechanism controlling the expression of macrophage functions during exposure to phorbol diesters.

Blood Bactericidal Activity↗
PubMed1981

The progeny of a single progenitor cell can develop characteristics of either a tissue or an alveolar macrophage.

Alveolar and peritoneal macrophages differ in their energy metabolism. Alveolar macrophages are mainly aerobic whereas peritoneal macrophages are mainly anaerobic in their energy generation. We investigated the question of whether these differences in metabolism are preprogrammed in subsets of macrophage precursors in the bone marrow, or develop in proliferating cells as a consequence of exposure to different tissue environments. The progeny of single mouse macrophage progenitor cells were grown in vitro for 4 days; the resultant colonies were divided into two roughly equal populations, which were cultured in either a high or low oxygen environment corresponding to that of the alveoli or tissues. Following 4 days incubation at 5% or 20% O2, the activities of the two glycolytic enzymes lactate dehydrogenase (LDH) and pyruvate kinase (PK) were two- to threefold higher in the half of the colonies grown in the low O2 environment, whereas the activity of the oxidative phosphorylative enzyme glutamate dehydrogenase (GDH) was two- to threefold higher in the half colony grown in the aerobic environment. Re-exposure of the cells from the low O2 environment to high O2 conditions for an additional 4 days caused a rise in the GDH activity and a decrease in the LDH and PK. The recovery of the GDH activity after the re-exposure was time dependent. Our results support the theory that macrophages arising from a single progenitor cell can develop different metabolic features depending on the O2 environment in which they mature. A single precursor cell can give rise to mature cells with metabolic characteristic of either alveolar or tissue macrophages.

Animals↗
PubMed1980

Phorbol diester-induced macrophage differentiation of leukemic blasts from patients with human myelogenous leukemia.

Phorbol esters, including 12-O-tetradecanoylphorbol 13-acetate (TPA), induce terminal macrophagelike differentiation of cells from human acute myelogenous leukemia lines. We report that myelogenous leukemia cells obtained from patients undergo macrophagelike differentiation after exposure to TPA. The myeloid leukemic cell cultured with TPA became adherent to charged surfaces with long filamentous pseudopodia; developed positive staining for alpha-napthyl acetate esterase, increased lysozyme secretion, reduced nitroblue tetrazolium, and acquired the ability to phagocytose candida. Cells from patients with lymphocytic leukemia did not become macrophagelike when cultured with TPA.

Cell Adhesion↗
PubMed1980

Monocyte function in rheumatoid arthritis.

Monocytes derived from peripheral blood of patients with rheumatoid arthritis (RA) had a marked defect in their bactericidal activity against Staphylococcus albus and Listeria monocytogenes; whereas the phagocytic capacity of monocytes from RA patients for both Staph. albus and Shigella flexneri was similar to that of monocytes from healthy subjects. There were no significant differences between the patient and control groups with regard to antibody dependent cellular cytotoxicity (ADCC) of monocyte against antibody-coated EL4 leukemia tumor cells. No correlation was observed between the rheumatoid factor (RF) titer in the serum of RA patients and the ADCC capacity of their monocytes. The ADCC of normal monocytes was reduced markedly following their incubation with serum from RA patients. It suggested that the defect in bactericidal activity in monocytes from RA patients may explain, at least in part, the susceptibility of RA patients to infections.

Adolescent↗
PubMed1979

Phagocyte functions in familial Mediterranean fever.

Monocytes derived from peripheral blood of patients with familial Mediterranean fever (F.M.F.) demonstrated lower phagocytic capacity for Shigella flexneri and depressed bactericidal activity against S. albus when compared to monocytes from healthy individuals. Treatment of patients with colchicine did not alter these functions. On the other hand, chemokinesis of PMN of F.M.F. patients was enhanced especially during attacks. Colchicine treatment decreased significantly the PMN chemotactic migration.

Adolescent↗
PubMed1979

Monocyte function in psoriasis.

Monocytes derived from the peripheral blood of psoriatic patients demonstrated a significantly higher phagocytic capacity (36 to 40%) for both 125I-labeled Shigella flexneri and 125I-labeled Staphylococcus albus compared with monocytes from healthy subjects. Monocytes from psoriatic patients showed a 2-to-4fold increase in bactericidal capacity against S. albus when compared with normal monocytes. However, the bactericidal capacity of monocytes from diphylline-treated patients did not differ from that of the control subjects. The antibody-dependent cellular cytotoxicity (ADCC) activity against EL4 tumor cells was found to be similar in both psoriatic patients and control subjects. It is postulated that these abnormalities of monocyte function in psoriasis are caused by a decreased cAMP/cGMP ratio similar to the decreased cAMP/cGMP ratio found in the lesional epidermis of this disease. It seems therefore, that the psoriatic abnormality is not confined to only one type of cell, the epidermal cell.

Adult↗
PubMed1979

Neutrophil chemotaxis in psoriasis.

Neutrophil chemotaxis was assessed in 69 psoriatic patients and 37 healthy human subjects. It was found to be significantly enhanced in 52 untreated patients. In 20 patients treated with an orally-administered phosphodiesterase inhibitor, Diphylline, neutrophil chemotaxis was normal. The enhanced chemotactic response of neutrophils from untreated patients with minimal skin lesions was at least equal to the response of those from patients with extensive skin lesions. Preincubation of normal human leukocytes with plasma derived from patients with widespread lesions markedly reduced their chemotactic activity. Plasma derived from patients with extensive skin lesions exhibited marked chemoattracting properties in comparison with plasma from healthy subjects. It is postulated that the basic intrinsic abnormality of neutrophil function in psoriasis could be caused by a decreased cyclic AMP/cyclic GMP ratio, similar to the decreased cyclic AMP/cyclic GMP ratio found in the lesional epidermis of this disease. Plasma factors which influence chemotaxis in psoriasis are related to the extent of the eruption and their effect is contrary to the effect of the basic intrinsic abnormality of psoriatic neutrophils.

Administration, Oral↗
PubMed1978

Enhanced chemotactic and phagocytic activities of leukocytes in psoriasis vulgaris.

Leukocytes derived from the peripheral blood of psoriatic patients demonstrated an enhanced chemotactic response compared with leukocytes from healthy subjects. No significant difference was detected between the chemotactic response of leukocytes from patients with minimal or no skin involvement and those from patients with extensive lesions. Psoriatic leukocytes also had a significantly higher capacity to engulf 125I labeled Shigella flexneri than control leukocytes. It is postulated that a decrease in the cyclic AMP/cyclic GMP ratio in psoriatic leukocytes, similar to the imbalance of these 2 cyclic nucleotides found in the lesional epidermis of psoriasis, might be the cause of their enhanced chemotactic and phagocytic activities.

Cyclic AMP↗
PubMed1978

The mode of interaction with macrophages of two ordered synthetic polypeptides which differ in their thymus dependency.

The mode of interaction with macrophages of two ordered synthetic polypeptides (Tyr-Tyr-Glu-Glu)-poly(DLAla)--poly(Lys), (T-T-G-G)-A--L, and (Tyr-Glu-Tyr-Glu)-poly(DLAla)--poly(Lys), (T-G-T-G)-A--L, which differ in their requirements for T-B cell co-operation in the process of antibody production, was compared. The binding of the two radiolabelled antigens to the surface of peritoneal adherent cells, their uptake by the cells and the rate of their degradation were investigated. Macrophages were found to be capable of degrading both poly-peptides with the same efficiency. (T-G-T-G)-A--L, the antigen which is less T-dependent, was bound to macrophage surfaces more readily than (T-T-G-G)-A--L, the T-dependent antigen, however, its uptake by the cells was found to be lower. Thus, (T-G-T-G)-A--L remains for a longer period in the form of a membrane bound polyvalent antigen.

Animals↗
PubMed1976

Studies on the relationships between the immunogenicity and catabolism of antigens and their binding to the surface of macrophages.

The relationship between immunogenicity of Shigella paradysenteriae, the branched synthetic polypeptide poly-L (Tyr, Glu)-polylpro-polyllys [(T, G)-Pro--L] and human albumin (HSA) interacting with macrophages and kinetics of antigen degradation and degree of binding to the cell surface was studied. Following thioglycollate inoculation into C57BL/6 mice, the peritoneal-stimllated macrophages had higher levels of hydrolases as compared to unstimulated cells. The lysates of the stimulated macrophages catabolized the three labeled antigens faster than did the lysates of unstimulatec cells. However, when degradation of labeled antigens by macrophage cells was assessed, no direct correlation could be demonstrated between the level of cell hydrolases and rate of (T, G)-Pro--L or HSA catabolism. The immunogenicity of antigens following their uptake by unstimulated and stimulated macrophages was determined by transfer of the antigen-bearing cells into irradiated and nonirradiated syngeneic recipients. No correlation was apparent between the rate of antigen degradation and the capacity to evoke a humoral response. Similarly, no correlation could be demonstrated between the amount of antigen bound to the macrophage cell surface and the immunogenicity of the antigen. It is suggested that neither the rate of antigen catabolism by macrophages nor the amount of antigen bound to the macrophage membrane is the sole factor which determines the immunogenicity of antigens interacting with macrophages.

Animals↗