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At least 289 records · Page 16Linked to original sources
PubMed1986

Effect of interleukin 1 on the expression of interleukin 2 receptor (Tac antigen) on human natural killer cells and natural killer-like cell line (YT cells).

The effect of interleukin 1 (IL 1) on the expression of interleukin 2 receptor (IL 2R/Tac antigen) on human natural killer (NK) cells and the NK-like cell line, YT was studied with the use of a fluoresceinated anti-IL 2R monoclonal antibody and a Spectrum III flow cytofluorometer. IL 2R was expressed on approximately 10% of NK cells. The expression of IL 2R on NK cells was increased to approximately 25% by the in vitro culture with monocytes or IL 1 and to a less extent by the culture with IL 2 or interferon-gamma (IFN-gamma). IL 2R was expressed on approximately 50% of YT cells without any stimulations. The expression of IL 2R on YT cells was increased up to almost 100% by the culture with IL 1 or monocytes, but not with IL 2, IFN-alpha, IFN-beta, IFN-gamma, or lectins such as concanavalin A and phytohemagglutinin-P. IL 1 absorbed with YT cells or murine thymocytes lost both IL 1 activity detected by the stimulation of murine thymocyte proliferative response and enhancing activity of IL 2R expression on YT cells, suggesting that IL 1 has both activities. However, the assay system of the expression of IL 2R on YT cells is much more sensitive than the stimulation of murine thymocyte proliferative response. By the kinetic study, the enhancement of IL 2R expression was induced by only a 2-hr incubation of YT cells with IL 1. This enhancement did not proceed at 4 degrees C or by the treatment of YT cells with actinomycin D or cycloheximide, suggesting that this enhancement is energy dependent and requires the synthesis of RNA and protein but not DNA. Thus IL 1 plays an important role for the regulation of the expression of IL 2R on NK cells, and IL 1-dependent IL 2R expression on YT cells may give us a good model for the study of the molecular mechanism of the regulation of IL 2R expression.

Antigens, Surface↗
PubMed2005

Transport mechanism for L-lactic acid in human myocytes using human prototypic embryonal rhabdomyosarcoma cell line (RD cells).

Monocarboxylate transporter (MCT), which cotransport L-lactic acid and protons across cell membranes, are important for regulation of muscle pH. However, it has not been demonstrated in detail whether MCT isoform contribute to the transport of L-lactic acid in skeletal muscle. The aim of this study was to characterize L-lactic acid transport using an human rhabdomyosarcoma (RD) cell line as a model of human skeletal muscle. mRNAs of MCT 1, 2 and 4 were found to be expressed in RD cells. The [14C] L-lactic acid uptake was concentration-dependent with a Km of 1.19 mM. This Km value was comparable to its Km values for MCT1 or MCT2. MCT1 mRNA was found to be present markedly greater than that MCT2. Therefore, MCT1 most probably acts on L-lactic acid uptake at RD cells. [14C] L-Lactic acid efflux in RD cells was inhibited by alpha-cyano-4-hydroxycinnamate (CHC) but not by butyric acid, a substrate of MCT1. Accordingly, MCT2 or MCT4 is responsible for L-lactic acid efflux by RD cells. MCT4 mRNA was found to be present significantly greater than that MCT2. We conclude that MCT1 is responsible for L-lactic acid uptake and L-lactic acid efflux is mediated by MCT4 in RD cells.

Base Sequence↗
PubMed1997

A calcium channel in human submandibular duct cell line, HSG cells, not regulated by P2U purinergic receptor-mediated intracellular calcium mobilization.

Signal transduction via P2 purinergic receptors was investigated in HSG cells, a continuous cell line originally derived from an irradiated human salivary gland. Ligand specificity for nucleotide receptors in HSG cells was investigated with various nucleotides and their analogues. Inositol 1,4,5-trisphosphate (IP3) production was significantly increased by ATP, UTP and ATP gamma S. The ligand specificity of this effect agreed well with that of the P2U purinergic receptor. On the other hand, 45Ca2+ influx was stimulated by ATP, UTP > ATP gamma S, ADP, UDP > ADP beta S > AMPPNP, GTP, TTP > CTP, GDP, TDP, AMPPCP, AMPCPP. This ligand specificity of 45Ca2+ influx was much broader than IP3 production. Also pertussis and cholera toxin had no effect on both IP3 production and 45Ca2+ influx by ATP or UTP. 3'-O-(4-benzoylbenzoyl)adenosine 5'-triphosphate (Bz-ATP) stimulates 45Ca2+ influx more effectively than IP3 formation. A 53-kDa membrane protein was photolabelled with [alpha-32P]Bz-ATP. This 53-kDa protein is a putative P2 purinergic receptor. In particular, the labelling was inhibited by a ligand profile that corresponded to that for 45Ca2+ influx. These findings suggest that nucleotides stimulate 45Ca2+ influx and IP3 formation by separate pathways via pertussis and cholera toxin-insensitive G proteins. Thus, in HSG cells, IP3 formation is coupled to the P2U subclass, while 45Ca2+ influx is coupled to another subclass, such as P2X, that regulates calcium channels.

Adenine Nucleotides↗
PubMed1981

Immunoglobulin glycopeptides from an IgG2b-producing mouse myeloma cell line and from variant cell lines.

A mouse myeloma cell line, 45.6.3, produces an IgG2b immunoglobulin (Ig) with 2 carbohydrate attachment sites on the heavy chains. One site is in the CH2 domain and the other in the VH region. The oligosaccharides at each site have different structures. The ratio of radioactive glucosamine incorporated in the VH compared with the CH2 oligosaccharide is approximately 1 to 3. In an attempt to understand this observation further, variant cell lines derived from 45.6.3 were isolated and their Ig were characterized. A ricin-resistant line, R4R1.5, has the same 2 attachment sites as the wild type, but the ratio of radioactive glucosamine in VH compared with CH2 was 1:1 and not 1:3 as in the wild type. This alteration is most probably due to cellular factors, since the Ig protein is unchanged. The M3.11 cell line produces an Ig with a polypeptide deletion involving the CH3 domain. In this Ig, a 3rd carbohydrate attachment site can be demonstrated. The percentage of radioactivity glucosamine in the CH2 domain compared with the total Ig is about 25% instead of 75% as in the wild type. These results suggest that the extent of glycosylation of different sites on Ig can be affected by both cellular factors and structural changes in the Ig protein.

Animals↗
PubMed2003

Intracellular proteins involved in Porphyromonas gingivalis-induced opsonophagocytic activities of a murine macrophage cell line (RAW264.7 cells).

The aim of this study was to determine the role of intracellular proteins in phagocytosis of opsonized Porphyromonas gingivalis by RAW264.7 cells, a murine macrophage-like cell line. This periodontopathogen was grown anaerobically and opsonized with an IgG2a murine monoclonal anti-P. gingivalis lipopolysaccharide antibody. RAW264.7 cells were preincubated with protein tyrosine kinase inhibitors (staurosporine and genistein), protein kinase C inhibitors (phorbol myristic acetate and bisindolylmaleimide), a serine/threonine phosphatase inhibitor (okadaic acid), a phosphatidylinositol 3-kinase inhibitor (worthmannin), phospholipase A2 inhibitors (bromophenacyl bromide and nordihydroguaiaretic acid), phospholipase C inhibitors (p-chloromercuriphenyl sulfonate and neomycin sulfate), an actin-filament depolymerizer (cytochalasin D), and a microtubule disrupting agent (colchicine). Inhibitor-treated macrophages were then incubated with the opsonized P. gingivalis and the phagocytosed cells determined microscopically. The results showed the percentage of the phagocytosed organisms decreased when the cells were preincubated with protein tyrosine kinase, protein kinase C, protein phosphatase and phosphatidylinositol 3-kinase inhibitors. Of interest, preincubation with phorbol myristic acetate for 30 min increased the ability of RAW264.7 cells to phagocytose the opsonized organisms. Phospholipase A2 and phospholipase C inhibitors only slightly reduced the number of phagocytosed organisms. The results indicated that opsonophagocytosis of P. gingivalis by RAW264.7 cells might be determined by the activation of protein tyrosine kinase, protein kinase C, protein phosphatases, and phosphatidylinositol 3-kinase inhibitor. Both phospholipase A2 and phospholipase C would appear to be involved to a lesser extent. The opsonophagocytosis of this periodontopathogen would also appear to be dependent upon actin and microtubule polymerization.

Animals↗
PubMed1991

Constitutive c-myc expression in an IL-3-dependent myeloid cell line suppresses cell cycle arrest and accelerates apoptosis.

In the murine interleukin 3 (IL-3)-dependent myeloid cell line 32D, down-regulation of c-myc and ornithine decarboxylase (ODC) expression is an immediate response to IL-3 deprivation. This is followed by an accumulation of cells in the G1 phase of the cell cycle, and eventual cell death. However, clones of 32D cells harboring an expression vector which constitutively expresses murine c-myc did not down-regulate ODC transcripts in response to IL-3 withdrawal, and they failed to G1 arrest. Moreover, in contrast to control cultures in which the majority of death occurred following G1 arrest, c-myc clones rapidly initiated a program of cell death characteristic of apoptosis following IL-3 deprivation, and their subsequent loss of viability occurred with accelerated kinetics. The premature induction of apoptosis in cells harboring a deregulated c-myc gene suggests that apoptosis may be an important mechanism in the elimination of hematopoietic cells harboring mutations, such as constitutive c-myc expression, which imbalance normal cell cycle regulatory controls.

Cell Cycle↗
PubMed1984

Regulation of transferrin receptors in human hematopoietic cell lines.

Cells grown in the presence of ferric ammonium citrate or hemin exhibited a concentration and time-dependent decrease in 125I-transferrin (Trf) binding. In contrast, cells grown in the presence of protoporphyrin IX or picolinic acid (an iron chelator) exhibited a marked increase in Trf binding. The decrease or increase in binding activity observed under these different conditions of culture reflected, respectively, a reduction or increase in receptor number rather than an alteration in ligand receptor affinity. Growth of the cells in the presence of saturating concentrations of apotransferrin only induced a slight reduction in receptor number. Investigation of the Trf receptors' turnover and biosynthesis clearly showed that iron and hemin decreased the synthesis of Trf receptors without any modification of the receptor turnover; in contrast, protoporphyrin IX and picolinic acid markedly increased the synthesis of Trf receptors. Our results suggest that hemin, iron, and protoporphyrin IX may represent the main molecules involved in the regulation of Trf receptors.

Antibodies, Monoclonal↗
PubMed1998

MHC class I bound peptides of a colon carcinoma cell line, a Ki-ras gene-targeted progeny cell line and a B cell line.

MHC class I associated peptides on cancer cells represent potential targets for CD8+ cytotoxic T cell activity against tumor cells. We eluted the naturally bound MHC class I peptides of a colon carcinoma cell line and compared them to peptides isolated from a B cell line and a slow-growing activated Ki-ras-disrupted colon cancer cell line. While we failed to detect any significant differences in class I associated peptides due to the presence or absence of activated Ki-ras in colon cancer cell lines, the colon cancer cell lines and B cell line presented vastly different peptide repertoires in the context of HLA-A*0201 molecules.

B-Lymphocytes↗
PubMed2002

Distinct patterns of mitogen-activated protein kinase phosphorylation and Epstein-Barr virus gene expression in Burkitt's lymphoma cell lines versus B lymphoblastoid cell lines.

In order to understand mechanistic relationships between signaling pathways regulating mitogen-activated protein kinase (MAPK) phosphorylation and Epstein-Barr virus (EBV) reactivation, we compared MAPK phosphorylation, and EBV reactivation and latency in Burkitt's lymphoma cell lines (BLCLs) versus B lymphoblastoid cell lines (LCLs). EBV was reactivated in the BLCLs Akata and Raji, and in a LCL OB-R33 cells after cross-linking surface immunoglobulin (sIg) with anti-Ig. After stimulation with anti-Ig, MAPK phosphorylation was strongly induced in all BLCLs and in a few LCLs, but not in other LCLs. MAPK was constitutively phosphorylated in most LCLs but not in BLCLs. Expression of EBNA2 and LMP1, and LMP2A was analyzed with both immunoblotting and RT-PCR. EBNA2 and LMP1 were expressed in most LCLs and in some BLCLs. LMP2A was expressed in all BLCLs and LCLs except Namalwa cells. To test the hypothesis that LMPI induces constitutive MAPK phosphorylation, the LMP1 expression vector was transfected into Akata cells. MAPK phosphorylation was not induced in such transfected cells. Our results indicate that BLCLs and LCLs respectively have distinct MAPK phosphorylation patterns, and that induction of MAPK phosphorylation correlates with EBV reactivation in a few cell lines but not in most of the tested cell lines.

Animals↗
PubMed1986

Generation of a monoclonal anti-GP70 antibody and characterization of its reactivity with various human cell lines and cells from leukemia-lymphoma patients.

Monoclonal anti GP-70 antibodies (BI) were generated in mice and used for screening of various malignant and non-malignant cell lines. The reactivity of these monoclonal antibodies was compared with that obtained with the polyclonal anti GP-70 antibody described in earlier studies [1-3]. The results indicated complete similarity in reactivity of both of the antibodies used. Furthermore, the reactivity of BI antibodies with cell samples obtained from a variety of leukemia and lymphoma patients and with peripheral blood samples from healthy blood donors was also very similar to the pattern of specificity described in earlier reports for the polyclonal preparation. From these studies we conclude that the monoclonal antibodies can substitute the polyclonal anti GP-70 antibodies in the diagnosis and subtyping of B-type leukemias and lymphomas.

Antibodies, Monoclonal↗
PubMed1999

Comparison between the clonogenic, MTT, and SRB assays for determining radiosensitivity in a panel of human bladder cancer cell lines and a ureteral cell line.

Using a series of human bladder cancer cell lines and an immortalised normal ureteral cell line, radiosensitivities measured by three different methods after a single dose of X-radiation are compared. Clear differences between cell survival curves obtained using the clonogenic, microtetrazoline (MTT) and sulforhodamine B (SRB) assays are shown. The most sensitive of the assays investigated was the clonogenic assay. The MTT and SRB assays were found to be relatively insensitive especially at lower radiation levels, suggesting that these assays may not be suitable for predicting therapeutic dose schedules in vivo, but will be important for investigating radio-sensitivity in cell lines with very low plating efficiencies. Each assay discriminated between a range of sensitivities in the cell lines examined, and with some minor differences, the ordering of sensitivities using the three assays was similar. Possible explanations for the differences between results obtained with the three assays are discussed.

Cell Survival↗
PubMed2000

Effect of selenium supplementation on the activities of glutathione metabolizing enzymes in human hepatoma Hep G2 cell line.

Cell culture is an important tool for studying injury to cells exposed to oxidative stress. The human hepatoblastoma derived Hep G2 cells retain their morphology and most of their function in culture and are therefore widely used as an in vitro model of human hepatocytes. Conventional cell culture media are deficient in selenium, which is essential for activation of glutathione peroxidase (GPx), a key enzyme in the defense against oxidative stress. Supplementation of the culture media with 1 microM sodium selenite increased the activities of total GPx by threefold and the selenium-dependent GPx by fourfold as compared to cells cultured in control media. The non-selenium-dependent GPx activity was unchanged. The activities of the other glutathione (GSH)-related enzymes were practically unchanged despite a tendency toward elevation. The activities of oxidized glutathione (GSSG) reductase and catalase increased by 22.4 and 27.4%, respectively. These relatively small increases did not carry statistical significance. Supplementation of tissue culture media with selenium may prove important, particularly for cell protection against oxidative stress.

Animals↗
PubMed2000

Adenovirus types 11p and 35p show high binding efficiencies for committed hematopoietic cell lines and are infective to these cell lines.

Hematopoietic cells are attractive targets for gene therapy. However, no satisfactory vectors are currently available. A major problem with the most commonly used adenovirus vectors, based on adenovirus type 2 (Ad2) or Ad5, is their low binding efficiency for hematopoietic cells. In this study we identify two adenovirus serotypes with high affinity for hematopoietic cells. The binding efficiency of prototype serotypes Ad4p, Ad11p, and Ad35p for different committed hematopoietic cell lines representing T cells (Jurkat), B cells (DG75), monocytes (U937-2), myeloblasts (K562), and granulocytes (HL-60) was evaluated and compared to that of Ad5v, the commonly used adenovirus vector, using flow cytometry. In contrast to Ad5v, which bound to less than 10% of the cells in all experiments, Ad11p and Ad35p showed high binding efficiency for all of the different hematopoietic cell lines. Ad4p bound to the lymphocytic cell lines to some extent but less well to the myelomonocytic cell lines. The abilities of the different serotypes to infect, replicate, and form complete infectious particles in the hematopoietic cell lines were also investigated by immunostaining, (35)S labeling of viral proteins, and titrations of cell lysates. Ad11p and Ad35p infected the highest proportion of cells, and Ad11p infected all of the cell lines investigated. The Ad11p hexon was expressed equally well in K562 and A549 cells. Jurkat cells also showed high levels of expression of Ad11p hexons, but the production of infectious particles was low. The binding properties of virions were correlated to their ability to infect and be expressed.

Adenoviruses, Human↗
PubMed2003

Increased calcium influx and ribosomal content correlate with resistance to endoplasmic reticulum stress-induced cell death in mutant leukemia cell lines.

Cell clones were derived by treatment of HL-60 cells with stepwise increasing concentrations of econazole (Ec), an imidazole antifungal that blocks Ca2+ influx and induces endoplasmic reticulum (ER) stress-related cell death in multiple mammalian cell types. Clones exhibit 20- to more than 300-fold greater resistance to Ec. Unexpectedly, they also display stable cross-resistance to tunicamycin, thapsigargin, dithiothreitol, and cycloheximide but not doxorubicin, etoposide, or Fas ligand. Phenotypic analysis indicates that the cells display increased store-operated calcium influx and resistance to ER Ca2+ store depletion by Ec. E2R2, the most resistant clone, was observed to maintain protein synthesis levels after treatment with Ec or thapsigargin. Expression of GRP78, an ER-based chaperone, was induced by these ER stress treatments but to equal degrees in HL-60 and E2R2 cells. By using microarray analysis, at least 15 ribosomal protein genes were found to be overexpressed in E2R2 compared with HL-60 cells. We also found that ribosomal protein content was increased by 30% in E2R2 as well as other clones. The resistance phenotype was partially reversed by the ribosome-inactivating protein saporin. Therefore, increased store-operated calcium influx, resistance to ER Ca2+ store depletion, and overexpression of ribosomal proteins define a novel phenotype of ER stress-associated multidrug resistance.

Anti-Bacterial Agents↗
PubMed1994

The immunosuppressive substance 2-chloro-2-deoxyadenosine modulates lipoprotein metabolism in a murine macrophage cell line (P388 cells).

A recently developed immunosuppressive substance, 2-chloro-2-deoxyadenosine (2-CdA), was reported to inhibit monocyte functions at low concentration. Because macrophages play a key role in the formation of atherosclerotic plaques, it was of interest to study the effect of 2-CdA on cellular lipid metabolism. For this purpose we have used a macrophage cell line (P388) to perform incubation studies in the presence of acetylated low density lipoprotein (Ac-LDL) and 2-CdA. The addition of 2-CdA, in concentrations ranging from 5-20 nM, induced a dose-dependent decrease in cellular cholesterol content and in the amount of extracellular [14C]oleic acid (OA) incorporated into the cholesteryl ester (CE) fraction. The effect was maximized at 20 nM 2-CdA with an 86% reduction in cholesterol esterification compared to controls (P < 0.008). To evaluate the mechanism of interaction of 2-CdA with cellular lipid metabolism, deoxycytidine (dCyt) and 3-methoxybenzamide (3-MOB), substances known to antagonize the effect of 2-CdA in different ways, were co-administered with 2-CdA. dCyt, a competitive inhibitor of dCyt kinase, which catalyzes phosphorylation to the active metabolite, antagonized the effects of 20 nM 2-CdA, producing significantly greater incorporation of extracellular [14C]OA into the CE fraction than in the presence of 2-CdA alone (P < 0.0086). Co-incubation with 2-CdA and the poly-ADP-ribose synthetase inhibitor 3-MOB, which is known to render cells resistant to 2-CdA toxicity by preventing cellular nicotinamide adenine dinucleotide (NAD)- and adenosine triphosphase-depletion, also reversed the effect of 2-CdA on lipid accumulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylation↗
PubMed2004

Inducible activity of ginger rhizome (Zingiber offifinale Rosc.) on the mRNA expression of macrophage-inducible nitric oxide (NO) synthase and NO production in a macrophage cell line, RAW264.7 cells.

We have investigated the effect of Zingiber offifinale Rosc. (ZOR) on macrophage-inducible nitric oxide (NO) synthase (macNOS) mRNA expression and NO production in RAW264.7 cells, a murine macrophage cell line; 100 microg/ml ZOR can induce macNOS mRNA expression, but induction effects at a dose below 10 microg/ml were weak or negligible. Kinetic studies showed that macNOS mRNA can be detected from 4 hours to 24 hours after dosing, with a peak at 8 hours. In accordance with the induction of macNOS mRNA expression, NO concentrations increased from 3.4 microM at 2 hours to almost 150 microM at 24 hours, reflecting a longer period of macNOS mRNA expression. The activity of ZOR can be considered to contribute, at least in part, to the beneficial effects of ZOR through the macNOS-mediated activation of the biodefense mechanism.

Animals↗
PubMed1994

HIV-1 gp41 binds to two proteins in cell culture supernatant of human B cell line Raji and monocyte cell line U937.

Based on our findings that HIV-1 gp41 can bind independently of CD4 to the human T cell line H9, B cell line Raji and monocytic cell line U937, as well as human peripheral blood mononuclear cells preferentially to B lymphocytes and monocytes, we examined whether soluble protein for HIV-1 gp41 binding exists in the cell culture supernatant of Raji and U937. Using HIV-1 recombinant soluble gp41 (sgp41; Env amino acid 539-684) attached to sepharose beads, the cell culture supernatants of Raji and U937 were absorbed. By SDS-PAGE of sgp41-eluates of these cell culture supernatants three protein bands of 70, 75 and 92kD were stained with Coomassie blue. By Western blot (ligand blot) analysis using sgp41, two protein bands of 70 and 75kD were observed in sgp41-eluates from Raji and U937 cell culture supernatants. These sgp41-eluates could inhibit the sgp41 binding to Raji and U937 cells. Our data indicate that Raji and U937 cells produce two soluble binding proteins for HIV-1 gp41.

B-Lymphocytes↗