PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “L Cells”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1978

Increased susceptibility to infection with herpes simplex virus types 1 and 2 of cold-adapted L cells.

L cells (L-As subline) have been adapted to a temperature of 4 degrees C. In the cold-adapted cells, designated LC3, greater amounts of infectious herpes simplex virus types 1 (HSV-1) and 2 (HSV-2) were synthesized than in the original L-As cells or in another control L-cell line. Two strains of HSV-1 reached higher infectious titres in LC3 cells grown at 36 degrees C than in those grown at 32 degrees C. The HSV-2 strain tested replicated in LC-3 cells grown at 32 degrees C better than at higher temperature. Increased reproduction of HSV in LC3 cells was not due to enhanced adsorption of virions on the cells as compared with control L cells. The multiplication of cold-adapted LC3 cells was and was not more intensive than of L-As and control L cells, respectively. The virological results are confronted with known physiological properties of cold-adapted cells.

Adaptation, Physiological↗
PubMed1979

[Immunological properties of malignant and nonmalignant L-cell sublines. I. Obtaining a malignant L-cell subline and its immunological cross reactivity with nonmalignant cells].

LS cells, the malignant subline of benign L cells, were obtained from L cells by selection carried out by means of their cultivation in the abdominal cavity of allogenic mice. When inoculated subcutaneously in a dose of 1 x 10(6) into the back, LS cells took and progressively grew in 70% of syngeneic animals. The preliminary immunization with L cells protected 30% of mice inoculated subsequently with L cells.

Animals↗
PubMed1975

Distinction between malignant L cells and normal mouse fibroblasts by rosette formation with sheep red blood cells.

Murine L cell fibroblasts, and derivatives were found to rosette with sheep red blood cells (SRBC). Primary fibroblast explants from the parent murine strain, C3H, did not possess this potential. No rosettes were observed with primary fibroblast explants from C57BL and B10Br mice, with a human fetal lung fibroblast, with baby hamster fibroblasts or their polyoma transormed derivative, or with a cell line, 1T-22, derived from BALB/c mice. Hybridization of 1T-22 and L cells, by Sendai virus-mediated cell fusion, suppressed the rosette potential of the L cell parent. The receptor for SRBC on L cells appears to result from the expression of a recessive characteristic.

Animals↗
PubMed1978

ATP-independent DNA synthesis in vaccinia-infected L cells.

Mouse L cells can be made permeable to exogenous nucleotides by a cold shock in 0.01 M Tris . HCl pH 7.8, 0.25 M sucrose, 1 mM EDTA, 30 mM 2-mercaptoethanol and 4 mM MgCl2. DNA synthesis in permeabilized L cells requires ATP whereas DNA synthesis in permeabilized L cells that are infected with Vaccinia virus is ATP-independent. Permeabilized L cells that are infected with ultraviolet-irradiated virus show a marked suppression of DNA synthesis which is not corrected by an excess of deoxynucleoside triphosphates and ATP. The ATP-dependent and ATP-independent processes of DNA synthesis are inhibited to the same extent by Mal-Net, pHMB, ara CTP and phosphonoacetate. Concentrations of daunorubicin and cytembena, which cause marked inhibition of the ATP-dependent enzymes, only cause partial inhibition of the ATP-independent enzymes.

Adenosine Triphosphate↗
PubMed1977

High molecular weight DNA intermediates synthesized by permeabilized L cells.

Mouse L cells rendered permeable to deoxynucleoside triphosphates synthesize DNA as an extension of replication forks that were active in the intact cells. The permeabilization process does not affect the size of the bulk cell DNA. Intermediate molecular weight DNA, synthesized in the intact cells, is neither degraded to small molecular weight DNA nor processed into bulk cell DNA following the permeabilization process. DNA synthesized by the permeable cells demonstrates a heterogenous distribution in alkaline sucrose gradients, with peaks at 26 S and 71 S. Pulse-chase experiments demonstrate that these two classes of DNA intermediates do not have a precursor product relation. They appear to be synthesized independently and at the same rate. The results are compatible with continuous synthesis of DNA along one template strand and discontinuous synthesis along the opposite strand. DNA synthesis in isolated L cell nuclei was compared to the process in permeabilized cells with the results demonstrating that the rate of DNA synthesis is slower in the nuclei than it is in the permeable cells. Alkaline sucrose gradient studies demonstrate that the DNA synthesized by isolated nuclei is smaller than the DNA synthesized by the permeable cells.

Buffers↗
PubMed1978

Inhibition of protein synthesis in mouse L cells by poly-L-ornithine.

A snythetic polypeptide, poly-L-ornithine (pLo; average molecular weight, 13,000), inhibited protein synthesis in mouse L cells in suspension culture. The inhibition was dependent upon both the concentration of pLo and the cell density, and the dose for half-inhibition was correlated with the cell density. Cell viability remained high in the concentration range of PLo causing inhibition of protein synthesis. This inhibition was prevented by addiction of calf serum with pLo, but not by washing the treated cells with serum or a high concentration of salt. PLo had no effect on protein synthesis in a cell-free system prepared from L cells or rabbit reticulocytes. The polysome profiles of cells treated with pLo were similar to those of control cells. Experiments on the effect of interchange of the ribosomes and supernatants of control and pLo-treated cells showed that the ribosomes from pLo-treated cells were inactive. The inactivation of these ribosomes was partially prevented by the presence of 120 mM K+ in the medium during pLo treatment. The inhibition of protein synthesis by pLo, therefore, may result from the binding of pLo to the cell membranes, causing leakage of intracellular K+ and thus inactivating ribosomes.

Blood↗
PubMed1976

[Reactions of hereophilic agglutinins with L-cells and different toxicity of anti-A HP to fibroblasts and L-cells in vitro].

The carbohydrate binding glycoprotein Anti-AHP binds to the plasma membrane of the (transformed) L-cell both in agglutination reactions and by the immunofluorescence technique. On the surface of (normal) mouse embryo fibroblast cells Anti-AHP receptors were not detectable. Anti-AHP is suitable as another marker for L cells. The random distribution of the binding sites at 4 degrees C changes with elevated temperatures (clustering, capping of sites). Anti-AHP inhibits the growth of L cells much more than that of fibroblasts. It does not act as a mitogen for the investigated cells.

Agglutination Tests↗
PubMed1976

DNA synthesis in permeabilized mouse L cells.

Mouse L cells are rendered permeable to nucleoside triphosphates by a cold shock with a near isotonic buffer. These cells retain their morphologic integrity and use exogenously supplied nucleotides and deoxynucleotides to synthesize RNA and DNA. The newly synthesized DNA is nuclear and is the product of semiconservative replication. Incorporation of deoxynucleotides into DNA by thymidine kinase-deficient cells were used to conform rigorously that the exogenously supplied deoxynucleotides were incorporated into DNA without intermediate processing through nucleosides. DNA synthesis requires the presence of Na+, ATP, all 4 deoxynucleotides, and Mg2+. The reaction is inhibited by N-ethylmaleimide, p-hydroxymercuribenzoate and actinomycin D. Hydroxy-urea and arabinosylcytosine do not inhibit the reaction whereas cytosine arabinoside triphosphate shows competitive inhibition with the deoxynucleotides. These findings indicate that the permeable cell system can be used for in situ evaluations of the replicative DNA polymerase using the endogenous DNA template.

Biological Transport↗
PubMed1978

DNA-binding proteins in the cytoplasm of vaccinia virus-infected mouse L-cells.

Mouse L cell fibroblasts were infected with vaccinia virus and labeled 2 to 3 h postinfection with [35S]methionine. Labeled proteins were fractionated on native and denatured DNA-cellulose columns and then analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Twenty-four 90,000 to 12,500, were detected. VDP-12A (molecular weight, 29,750) had affinity for denatured but not native DNA, and its synthesis was dependent on viral DNA replication. VDP-20 (molecular weight, 41,000) bound very tightly to native and denatured DNA and was displaced only after boiling the protein-DNA-cellulose matrix in 1% sodium dodecyl sulfate. VDP-8,-11,-12,-13, -and-14 behaved electrophoretically like the polypeptide species previously shown to be present in DNA-protein complexes prepared from infected cells. The molecular weights of VDP-10 (50,000), VDP-11 (36,000), and VDP-8 (67,000) were similar to the polypeptide subunits of polyadenylate polymerase and phosphohydrolase I, enzymes purified from virions which have also been shown to have affinity for DNA.

Cytoplasm↗
PubMed1977

Contamination of human melanoma cell lines by mouse L cells.

Five of 8 cell lines from human melanomas originally established elsewhere were found to consist exclusively of mouse cells when examined in our laboratory some months after their receipt. Cytogenetic studies, including G- and C-banding, showed that the mouse cells in all cultures had originated from a single cell line, identified as the L-line. Contamination probably occurred, one year before its discovery, in a laboratory where L cells and human melanoma cells were briefly kept in the same incubator.

Animals↗
PubMed1979

Mechanisms of protein degradation in growing and non-growing L-cell cultures.

L-cells prelabelled with [14C]leucine and [3H]thymidine were placed in either fresh growth medium (minimal essential medium with 10% serum) or stepdown medium (minimal essential medium) for 3 days. The 14C/3H ratio remained constant in the growing cultures and decreased in the stationary-phase cultures, indicating no protein turnover in growing cultures and a degradative rate of 0.6%/h in the stationary-phase cultures. Media analysis, however, indicated that 14C-labelled proteins were being degraded at approx. 1.2%/h in growing cultures and 1.7%/h in stationary-phase cultures. Additional studies indicated that a subpopulation of L-cells in the monolayer, comprising approx. 20--30% of the total, were lost in the original processing procedure. Experiments in which recoveries approached 100% by fixation of the monolayer in situ indicated that a protein-degrading subpopulation accounted for all the observed proteolysis in the growing cultures. Proteolysis in these cultures was only partially inhibited with NH4Cl, indicating that only a small part of the protein degradation was occurring in an activated lysosomal-autophagic system. NaF produced a more effective inhibition of proteolysis, but we were not able to distinguish whether this effect was on an ATP-requiring basal-turnover mechanism or a direct effect on unregulated activity of proteinases in the cell hyaloplasm. However, NH4Cl inhibited the proteolysis induced when cells were placed in stepdown medium, suggesting that the induced proteolysis was occurring via the autophagic system. We conclude that L-cells exist in at least two states with respect to protein degradation: (a) a subpopulation that is actively replicating and does not degrade cellular proteins, and (b) a second subpopulation of cells, derived from the preceding one, which degraded most of their labelled proteins, are not capable of further replication, and are not sedimented in an iso-osmotic EDTA buffer solution. In addition, proliferating L-cells, when placed in stepdown medium, begin to degrade cell protein through a mechanism involving autophagolysosomes.

Ammonium Chloride↗
PubMed1979

Structure of tumor antigen on hybrid cells between mouse mammary ascites tumor and mouse fibroblast L cells.

Somatic cell hybrids between mouse fibroblast L cells and MM2 mouse mammary ascites tumor grown in BALB/c mice were isolated and the structures of tumor-associated surface antigen of the hybrid cells, and parental MM2 and mouse L cells were investigated by the methods of radioiodination of membrane proteins, immunoprecipitation with a specific antiserum against tumor-associated surface antigens of MM2 tumor (anti-MM2 serum), and sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Two molecules of 105,000 and 76,000 daltons were detected on the MM2 cell surface, but no MM2 tumor antigen was detected on the mouse L cells. On the hybrids between these two kinds of cells, in addition to the two MM2 tumor antigens, molecules of 48,000-51,000 and 12,000 daltons were observed. On Sendai-virus-infected mouse L cells only a molecule of 68,000 daltons was detected by the anti-MM2 serum, and furthermore this molecule was also detected by normal mouse serum, indicating that antibodies against Sendai virus were contaminating in both the anti-MM2 and normal mouse sera used, and thus the molecules detected on the hybrid cells were distinguishable from possible viral components of Sendai virus on the hybrid cells. The results indicate that somatic cell hybrids between mouse L cells and MM2 tumor grown in BALB/c mice expressed on their cell surface the molecules that were not exposed on either parent cell. The experiments comparing newly detected molecules with the H-2 antigen suggested that they were similar to H-2 in their electrophoretic pattern.

Animals↗
PubMed1977

Toxicity of low and moderate multiplicities of Chlamydia psittaci for mouse fibroblasts (L cells).

When mouse fibroblasts (L cells) were infected in suspension or in monolayer with 10 to 100 50% infectious doses (ID(50)) of Chlamydia psittaci (6BC) per host cell, they showed signs of damage 24 to 48 h later. Host-cell injuries were termed multiplication dependent when both the ingestion and subsequent reproduction of C. psittaci were required; when only ingestion but not replication was needed, the injuries were considered to be multiplication independent. The time that the injury was first apparent, as well as its final magnitude, was proportional to the multiplicity of infection. When L cells ingested infectious or ultraviolet-inactivated C. psittaci, damage was manifested by failure to exclude trypan blue, by leakage of lactic dehydrogenase, by inhibition of reproduction as measured by ability to form colonies, by inhibition of protein and deoxyribonucleic acid synthesis, and eventually by cell disintegration. Infectious, but not ultraviolet-killed, chlamydiae stimulated host-cell glycolysis. Heat-killed chlamydiae were without measurable toxicity. The time of appearance of host-cell injury was always earlier, and its terminal magnitude always greater, with infectious inocula than with ultraviolet-inactivated ones. The multiplication-independent toxicity of ultraviolet-killed C. psittaci disappeared with inocula of less than 10 ID(50) per L cell, but an inoculum of only a single ID(50) of infectious chlamydiae per host cell injured most of the cells it infected, as evidenced by increased trypan blue staining and decreased efficiency of colony formation. The toxicity of multiplicities of infection between 10 and 100 ID(50) of infectious C. psittaci per host cell was the sum of both multiplication-dependent and -independent components. The effects of chloramphenicol and isoleucine deficiency on the ability of C. psittaci to injure L cells suggested that some synthesis of protein by both parasite and host may be essential for expression of multiplication-independent chlamydial toxicity. The failure of infectious chlamydiae to stimulate host-cell glycolysis in the presence of cycloheximide suggested that this multiplication-dependent consequence of chlamydial infection was also dependent on protein synthesis by the host.

Bacterial Proteins↗
PubMed1979

Isolation and properties of LC3 cells, a new cold-resistant L cell subline.

LC3 cells, selected from the L-As cells by repeated exposures to 4 degrees C for 3--6 weeks with intermittent reincubations at 36 degrees C, differ from the initial population by better survival at 4 degrees C, more rapid recovery at 36 degrees C, a higher multiplication at subnormal temperature, a higher sensitivity to supranormal temperature, increased cell size at 36 degrees and 4 degrees C, and higher oxygen consumption at 36 degrees C. These properties are the same as those described in our previously isolated cold-resistant L cell variants and are typical for the resistance to low temperature. The increased activity of alkaline phosphatase, detected in two of our cold-resistant L cell sublines, was not found in the LC3 cells and has thus no relation to decreased cold sensitivity.

Animals↗