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Query: UNIPROT:P00750 (PLA)
 16,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Macrophages were obtained by peritoneal lavage from untreated mice or from mice which had received either Brewer's thioglycollate broth or a suspension of streptococcus A cell walls intraperitoneally 4 days before. 3 h after harvesting, adherent cells from untreated mice were allowed to phagocytose zymosan, formaldehyde-treated sheep erythrocytes, or latex beads. Phagocytosis was stopped after 1 h and culture was continued for up to 10 days. Phagocytosis of zymosan or sheep erythrocytes triggered the immediate release of lysosomal glycosidases, stimulated the synthesis of cellular lactate dehydrogenase, and induced the delayed production and secretion of plasminogen activator . No such changes were observed upon phagocytosis of latex. Although all three particles used were phagocytosed, only zymosan and sheep erythrocytes stimulated glucose oxidation via the hexose monophosphate shunt. Similar findings were obtained in macrophages elicited with streptococcus A cell walls after zymosan phagocytosis. Thioglycollate-elicited macrophages, however, which were already secreting lysosomal hydrolases and plasminogen activator, could not be activated further by zymosan. The results of this study show that macrophages become activated after phagocytosis of particles that stimulate the activity of their hexose monophosphate shunt. The triggering event appears to be the burst of shunt activity itself or shunt-related biochemical reactions rather than phagocytic uptake per se or particle-dependent complement activation by the alternative pathway. Once initiated, macrophage activation proceeds independently of the intracellular fate of the ingested material .
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PMID:Role of phagocytosis in the activation of macrophages. 72 42

We have examined the phosphorylation state of five proteins known to become phosphorylated on tyrosine during transformation by Rous sarcoma virus by using cells infected with a panel of partially transforming mutant viruses. Situations of viral mutant and growth temperature were found in which phosphorylation of some proteins occurred more extensively than that of others, indicating that mutations in the src gene had affected the specificity of pp60src for some of its substrates as well as affecting the activity of the enzyme. To obtain insight into the biological functions of these phosphorylations, comparisons were made between the degree of phosphorylation of these proteins and the expression of various indicators of the transformed phenotype. The data suggest that phosphorylation of proteins l, p, and q (Mr of 46,000, 39,000 and 28,000, respectively) is not sufficient to induce changes in adhesiveness, hexose transport or morphology. The phosphorylation of protein p or l or total phosphotyrosine content correlated well with the production of plasminogen activator, and the phosphorylation of proteins l and q correlated well with increased hexose transport. However, even when good correlations were observed, significant exceptions were sometimes noted. It thus remains possible that some phosphorylations on tyrosine observed in Rous sarcoma virus-transformed cells are not causally related to the expression of the measured parameters of transformation.
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PMID:Phosphotyrosine-containing proteins and expression of transformation parameters in cells infected with partial transformation mutants of Rous sarcoma virus. 618 22

Fifteen transformation defective sensitive mutants of Rous sarcoma virus have been investigated to see if the expression of the pp60src-associated protein kinase activity correlated with other parameters of transformation such as altered growth control, morphological changes, increased hexose transport, and increased plasminogen activator protease synthesis. The expression of a protein kinase activity paralleled or preceded the onset of other parameters of transformation with but one exception: altered control of cell growth. The stability of the pp60src molecule in mutant-infected cells at the nonpermissive temperature was investigated with the finding that mutant pp60src did not show an increased turnover at the nonpermissive temperature as compared to wild type virus pp60src. Furthermore, it could be shown that pre-existing pp60src in mutant-infected cells maintained at the non-permissive temperature became activated after temperature shift to the permissive temperature. Temperature shift performed under conditions of inhibition of new protein synthesis with cycloheximide, puromycin, or emetine was followed by greatly increased protein kinase activity, and a parallel phosphorylation of pp60src itself in tyrosine residues. Morphological features of transformation could be demonstrated likewise under conditions of inhibition of protein synthesis.
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PMID:In vitro transformation with Rous sarcoma virus and the pp60src-associated protein kinase. 626 96

In order to investigate a possible correlation between in vitro transformation and tumorigenicity in ovo, a new temperature-sensitive class T mutant of Rous Sarcoma Virus was isolated with a lower (39 degrees 5C) restrictive temperature for morphological transformation. This lower restrictive temperature was compatible with the survival of chicken and duck eggs for the tumorigenicity studies. In chicken embryo fibroblasts (CEF) infected by this new mutant, PA 17, and cultured at 39 degrees 5C, increase of hexose uptake, plasminogen activator production and anchorage-independent growth were only partially restricted, requiring incubation at 41 degrees 5C for a complete shut-off. Tumorigenicity in chicken and duck eggs inoculated with CEF infected and transformed by PA 17 was restricted at 39 degrees 5C, correlating well with the restriction of morphological transformation at this temperature. The kinase activity of the transforming protein pp60src in lysates of PA 17 infected cells cultured at permissive or restrictive temperatures was labile in RIPA buffer, as in the case of some previously examined ts T mutants. In the non-ionic detergent NP40 buffer, the kinase activity of PA17 infected cell lysates was better conserved and showed a moderate temperature dependence. These results suggest that, in spite of the correlations between the transformed cell phenotype in vitro and cell tumorigenicity in ovo, it is difficult to establish a quantitative relationship.
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PMID:A ts T mutant of Schmidt Ruppin strain of Rous sarcoma virus restricted at 39.5 degrees C for the morphological transformation and the tumorigenicity of chicken embryo fibroblasts. 627 5

We have isolated and characterized mutants of Rous sarcoma virus which induce some parameters of transformation but fail to fully induce other parameters. We believe these mutants code for a pp60src which phosphorylates some targets well but phosphorylates others poorly. Using these mutants, we examined the phosphorylation of a 36,000 Mr protein which is phosphorylated on a tyrosine in cells transformed by Rous sarcoma virus, in an attempt to correlate this phosphorylation with the expression of specific transformation parameters. We found that phosphorylation of the 36,000 Mr protein was neither necessary nor sufficient for loss of fibronectin or for loss of density-dependent inhibition of growth. Phosphorylation of the protein was not sufficient for morphological alterations, increased hexose transport, or loss of adhesiveness. For the parameters measured, the best correlation was with increased plasminogen activator. In addition, it is noteworthy that cells infected with the mutant CU2 displayed low levels of phosphorylation of the 36,000 Mr protein and also were deficient in anchorage-independent growth and tumorigenicity, raising the possibility that the phosphorylation of the 35,000 Mr protein may be required for malignant growth properties.
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PMID:Phosphorylation of a 36,000 Mr cellular protein in cells infected with partial transformation mutants of rous sarcoma virus. 628 26

Under conditions employed in our laboratory, tumors which are induced by avian sarcoma virus (ASV) usually grow progressively for several weeks and then regress. In order to further understand the basis for tumor regression in this model, we compared avian sarcoma cells which were cultured from tumors at different stages of development in terms of various phenotypic properties. The results indicate that tumor cells which are derived from progressively-growing sarcomas are rapidly growing, produce large quantities of the enzyme plasminogen activator, and have much in common generally with chicken embryo fibroblast (CEF) cells that have been transformed by ASV. In contrast, tumor cells that are obtained from regressors have elevated levels of hexose transport, grow very slowly, are greatly enlarged and display properties that are characteristic of senescent cells in culture.
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PMID:Phenotypic differences between tumor cells derived from different stages of neoplastic growth. 628 92

Cell line CEC-32 and clone LSCC-H32 were established from primary chicken embryo cells spontaneously but not experimentally transformed at 32 degrees C. The lines consisted of fibroblastoid and polygonal cells and had a subtetraploid karyotype of 2N = 130 to 140. The cells showed increased plating efficiency and metabolic activities as demonstrated by hexose uptake and plasminogen activator assay. The established cells produced avian lymphoid leukosis viruses of subgroups A and B. The virus released from LSCC-H32 cells induced lymphoid leukosis in inoculated chickens 18 to 22 wk post infection (PI). The cells have been carried in continuous culture for 285 passages and they appeared to grow indefinitely. They were efficiently used to propagate several animal viruses and to titrate chicken interferon.
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PMID:Establishment and characterization of chicken embryo fibroblast clone LSCC-H32. 629 61

The effect of the cyclooxygenase inhibitors, indomethacin and diclofenac, and of PGE2 on either resting or stimulated macrophages was investigated. Peritoneal macrophages were obtained from untreated mice and cultured for 10 days. Macrophage activation was induced by zymosan phagocytosis and was monitored by testing for plasminogen activator secretion and the cellular levels of lactate dehydrogenase, beta-glucuronidase and alkaline phosphodiesterase I. It was found that cyclooxygenase inhibitors activate resting macrophages and enhance the degree of activation obtained after zymosan phagocytosis. Addition of exogenous PGE2, on the other hand, had the opposite effect, it suppressed activation induced either by cyclooxygenase inhibitors, phagocytosis or a combination of both. Cyclooxygenase inhibitors and PGE2 did not affect the hexose monophosphate shunt activity of resting macrophages and had only a minor effect on the respiratory burst occurring during zymosan phagocytosis. It appears, therefore, that the observed changes in the state of activation of the macrophages are not related to hexose monophosphate shunt activity. The described effects suggest that PGE2 and possibly other cyclooxygenase products may function as inhibitory feed-back regulators of macrophage activation.
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PMID:Effects of cyclooxygenase inhibitors and prostaglandin E2 on macrophage activation in vitro. 679 85

Resident peritoneal macrophages were obtained from untreated mice and were cultured in medium 199 with or without 5% acid-treated fetal bovine serum. Three hours after harvesting, redox compounds--i.e., methylene blue, methyl viologen, or nitro blue tetrazolium--were added to the cultures of adherent cells. After 1 hr, the cells were washed and culturing was continued in the absence of redox compounds. The effects of the redox compounds were tested by assaying for hexose monophosphate (HMP) shunt activity and for plasminogen activator secretion, and the results were compared with the effects induced by phagocytic stimuli. Methylene blue caused a concentration-dependent stimulation of the HMP shunt, whereas methyl viologen and nitro blue tetrazolium were ineffective. Shunt stimulation by methylene blue was followed, after a lag of 2-4 days, by plasminogen activator secretion. The rate of secretion was dependent on the methylene blue concentration used. Methyl viologen and nitro blue tetrazolium were again ineffective, whereas phagocytosis of zymosan or sheep erythrocytes, which stimulates the HMP shunt, induced plasminogen activator secretion at rates similar to those induced by methylene blue. These results add further evidence to our hypothesis that the HMP shunt-dependent metabolic burst is involved in macrophage activation. Because methylene blue mimics the action of zymosan it appears that shunt stimulation by itself initiates the activation process independently of phagocytosis.
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PMID:Induction of plasminogen activator secretion in macrophages by electrochemical stimulation of the hexose monophosphate shunt with methylene blue. 692 34

We have investigated the effects of the tumor promoter 12-0-tetradecanoyl-phorbol-13-acetate (TPA) on plasminogen activator production, hexose transport and metabolism, and the incorporation of choline into the acid soluble pool and into phosphatidylcholine in suspension cultures of mouse L, mouse P388 leukemia, human HeLa, and Chinese hamster ovary cells, and in monolayer cultures of baby hamster kidney (BHK), mouse 3T3, mouse 3T6, and mouse P388D1 macrophage-like cells. BHK, 3T3, P388D1, and P388 cells produced plasminogen activator constitutively, but no significant production was observed in the other cell lines. Plasminogen activator production was induced or stimulated by TPA only in P388 cells (10- to 20-fold by 100 ng TPA/ml). On the other hand, phosphatidylcholine synthesis was stimulated by TPA only in HeLa cells, and hexose transport, as measured with 3-0-methyl-D-glucose, only in 3T3 and P388D1 cells, as well as in human lymphocytes. The stimulation of hexose transport occurred more rapidly than the induction of plasminogen activator production and seemed to be part of the mitogenic response of cells to TPA treatment. A stimulation of deoxyglucose uptake was similarly limited to 3T3 and P388D1 cells. A significant decarboxylation of carbon 1 of deoxyglucose occurred in P388 and P388D1 cells, but not in Novikoff cells, and any decarboxylation that occurred was not stimulated by TPA. The results indicate that the various investigated responses of cells to TPA are unrelated and occur independent of each other. The time courses of the biochemical responses also differ significantly.
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PMID:Lack of correlation between effects of tumor promoter TPA on plasminogen activator production, phosphatidyl choline synthesis, and hexose transport in mammalian cell culture systems. 719 88


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