Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The receptor for gp70 envelope glycoprotein of murine ecotropic leukemia virus is essential for virus entry into the host cell and has been recently demonstrated to function as a cationic amino acid transporter. In the experiments reported herein, we compared the gene expression of the murine ecotropic retroviral receptor (ERR) and its human homolog (H13) in rapidly proliferating cells versus resting cells using four different systems. (i) The expression of ERR gene is enhanced during activation of T and B lymphocytes by concanavalin A and lipopolysaccharide, respectively. Similar enhancement is observed by adding phorbol 12-myristate 13-acetate (PMA) or calcium ionophore (A23187). These phenomena appear to involve protein kinase C; two PMA analogs, 4 alpha-phorbol and 4 alpha-PMA, lacking the ability to activate protein kinase C fail to induce elevated levels of gene expression, and the protein kinase C inhibitor, H7 [1-(5-isoquinolinylsulfonyl)-2-methylpiperazine dihydrochloride[, inhibits the enhancement induced by PMA. (ii) Friend murine leukemia virus induces rapid splenomegaly, and acute erythroleukemia in sensitive mice. Concomitantly with splenomegaly, ERR gene expression in spleen cells increases dramatically. (iii) The level of expression of the ERR or H13 gene in a variety of tumor cells is highly elevated compared with the level in noncancerous cells. (iv) H13 gene expression decreases upon terminal differentiation of the human promyelocytic leukemia cell line HL-60 into granulocytes or macrophages by dimethyl sulfoxide or PMA, respectively. These results suggest that ERR and H13 genes play an important role in cellular proliferation.
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PMID:Enhanced gene expression of the murine ecotropic retroviral receptor and its human homolog in proliferating cells. 131 7

The effects of 17 beta-estradiol (E2), progesterone (P) and testosterone (Te) on cell differentiation in the HL-60 promyelocytic leukemia cells after treatment with 1 alpha, 25-dihydroxyvitamin D3 [1,25-(OH)2D3] and those on interleukin-1 beta (IL-1 beta) production by HL-60 cells in response to lipopolysaccharide (LPS) were investigated. Neither E2 (10(-10) to 10(-7) M), P (10(-9) to 10(-6) M) nor Te (10(-10) to 10(-7) M) affected monocytic differentiation as assessed by reactivity with OKM14 monoclonal antibody and alpha-naphthyl acetate esterase activity. Pretreatment of HL-60 cells with 1,25-(OH)2D3 enhanced their ability to produce IL-1 beta in response to subsequent exposure to LPS, although 1,25-(OH)2D3 by itself did not induce IL-1 beta production by HL-60 cells. This priming effect of 1,25-(OH)2D3 was augmented by the addition of E2 and Te at physiologic concentrations, but not by that of P. E2, P and Te at physiologic concentrations enhanced IL-1 beta production by HL-60 cells that were pretreated with 1,25(OH)2D3 and stimulated by LPS. The increasing rate of IL-1 beta production by the addition of E2 and Te was higher when added with LPS than when added with 1,25-(OH)2D3. These findings suggest that enhancing effects of sex steroids in IL-1 beta production by monocyte/macrophage lineage cells.
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PMID:Effects of sex steroids on cell differentiation and interleukin-1 beta production in the human promyelocytic leukemia cell line HL-60. 147 72

The regulation of the 55-kDa TNF receptor (TNF-R) mRNA synthesis, membrane expression, and TNF binding factor (BF) release was examined in resting and activated human monocytic THP-1 and human promyelocytic leukemia HL-60 cells in vitro. Cells were activated with phorbol myristate acetate (PMA) and bacterial lipopolysaccharide (LPS). TNF alpha cytolytic activity in the supernatant of THP-1 cells stimulated by PMA began to appear at 4 hr, reached a peak at 8 hr, and declined by 12 hr. For THP-1 cells stimulated with LPS, the peak of TNF alpha activity appeared at 4 hr and then declined. TNF alpha-binding sites on the cell membrane were down-regulated within 1 hr after PMA and LPS treatment and then reappeared 12 hr later. Fifty-five-kilodalton TNF-R mRNA expression during this time period did not correlate with the level of membrane TNF-binding site expression. Additional studies indicated the presence of a 30-kDa TNF-BF in the supernatants which appeared after 24 hr. These data suggest that activated THP-1 and HL-60 cells are capable of releasing TNF-BF into the supernatant and this material may be involved in the control of secreted TNF alpha activities.
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PMID:The regulation of TNF receptor mRNA synthesis, membrane expression, and release by PMA- and LPS-stimulated human monocytic THP-1 cells in vitro. 165 85

A growth-inhibitory (GI) factor, that specifically inhibits the growth of mouse monocytic leukemia cells, was found in conditioned medium of mouse lung tissue, but not in that of mouse brain, heart, liver, or kidney tissue. Conditioned medium of spleen or bone marrow cells had low GI activity. Pulmonary macrophages were as active as peritoneal and bone-marrow-derived macrophages in production of the GI activity. The GI factor inhibited the growth of murine monocytic leukemia cell lines Mm-A and J774.1, but scarcely inhibited the growth of other mouse cell lines, such as a myeloblastic leukemia cell line (M1), a Friend erythroleukemia cell line (745A) and a mammary carcinoma cell line (FM3A). It had no significant effect on the growth of human monocytic leukemia cell lines U937 and THP-1 or on the HL-60 promyelocytic leukemia cell line. These results suggest that the GI factor produced by mouse lung tissue preferentially inhibits the growth of mouse monocytic cells. The GI factor was found to be a proteinaceous substance with a molecular mass of 25 kDa. On chromatofocusing, the GI activity was eluted with Polybuffer 96/acetic acid at pH 7.2-7.5. The GI activity was not significantly decreased by heat treatment at 56 degrees C for 30 min or acid treatment (0.01 M HCl, 14 h), but the GI activity in glycosidase-treated conditioned medium of lung tissue was lost on heat treatment. The GI activity could not be neutralized with anti-(interferon alpha + beta) antibody. The activity was produced constitutively by lung tissues and its production was not stimulated appreciably by lipopolysaccharide, lectin, or poly(I).poly(C). The GI factor appears to be a cytokine unrelated to known cytokines such as tumor necrosis factor, interleukin-1, transforming growth factor beta, and interferons. These results suggest that the GI factor may be involved in negative feedback regulation of macrophage production in steady-state conditions in the lungs.
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PMID:Normal mouse lung tissue produces a growth-inhibitory factor(s) preferential for mouse monocytic leukemia cells. 248 Aug 47

Human promyelocytic leukemia cells, when differentiated into macrophages by treatment with phorbol myristate acetate, secrete a cytolytic factor. Enhanced production was achieved when the cultures were treated with bacterial lipopolysaccharide (LPS). Production of the factor was inhibited when cultures were treated with dactinomycin immediately after LPS treatment. Tritirachium alkaline proteinase treatment inactivated the factor, indicating that it has an essential protein moiety. The molecular weight was found to be approximately 40,000 by Sephacryl S-200 gel filtration. The factor was stable at 56 degrees C for 30 minutes, but 80% of the activity was inactivated at 70 degrees C in 30 minutes. The factor was destroyed (96%) by dialysis against 0.01 M HCl (pH 2) for 14 hours. The cytolytic factor had little activity on normal fibroblasts, but it was able to significantly kill transformed cells in vitro.
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PMID:Production of a cytotoxin from phorbol myristate acetate-treated human promyelocytes. 658 36

Studies on the effect of retinoic acid (RA) and 1,25-dihydroxyvitamin (D3) on the differentiation of leukemic cells have provided insight into the cellular and molecular mechanisms underlying hematopoietic cell differentiation. We have evaluated the combined effect of these chemical inducers on the differentiation of HL-60 and AML-193 promyelocytic leukemia cell lines. Simultaneous RA+D3 addition potentiated leukemic cell maturation up to mature phagocytic cells. Interestingly, AML-193 cells induced with D3 and RA displayed a typical neutrophilic morphology while exhibiting properties specific to monocytic cells, e.g., high expression of CD14 membrane antigen, capacity to bind bacterial lipopolysaccharide, and monocytic-specific esterase activity; this hybrid granulomonocytic (GM) phenotype was not observed upon initial incubation with one inducer and later addition of the other. Parallel control studies were performed with purified normal GM progenitors, triggered by interleukin 3+GM-colony-stimulating factor (CSF) in FCS-rich or -free clonogenic culture, by GM-CSF+M-CSF in FCS-rich clonogenic culture, and by M-CSF in liquid suspension culture. The progenitors grown in the first condition generate exclusively G clones, even upon addition of D3 and/or RA. The progenitors grown in the second and third culture conditions generate either G and M clones (second culture condition) or a population of cells composed by a majority of monocytes (third culture condition); the D3 addition did not modify this differentiation pattern, whereas RA or RA+D3 addition elicited a marked inhibition of monocytic differentiation. These observations suggest that the development of a hybrid GM phenotype is restricted to the progeny of bipotent GM leukemic precursors.
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PMID:Combined vitamin D3/retinoic acid induction of human promyelocytic cell lines: enhanced phagocytic cell maturation and hybrid granulomonocytic phenotype. 764 32

When rabbit alveolar macrophages were treated with phorbol-12-myristate-13-acetate (PMA) and lipopolysaccharide (LPS), the synthesis of interleukin-1 (IL-1), as well as tumor necrosis factor (TNF), was greatly increased. These inducible cytokines were subjected to cloning by the differential colony hybridization method and the subsequent mRNA hybridization-translation assay. Cloned rabbit IL-1 cDNA was disclosed to encode the sequence of the counterpart of the mouse IL-1 alpha. This cDNA was used as a hybridization probe to screen a human cDNA library which was constructed from induced HL-60 cells, a human promyelocytic leukemia cell line. Isolated human IL-1 alpha cDNA was shown to direct the synthesis of a polypeptide with IL-1 activity in E. coli expression system. The chromosomal gene for human IL-1 alpha was isolated and characterized to elucidate the structural organization of this gene. To identify the region that is essential for regulating IL-1 alpha gene expression, various CAT (chloramphenicol acetyltransferase) fusion plasmids were constructed and analysed for their ability to direct CAT synthesis in a transient expression system. The unpublished results obtained in the early stages of these experiments are also presented and discussed in this review.
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PMID:Molecular studies on interleukin-1 alpha. 772 86

The capability of human promyelocytic leukemia cells HL60 to be induced to differentiate to various stages along the monocytic or myelocytic pathway was exploited for investigation of the uptake of selected photosensitizers by diverse types of cells of the same origin. The results showed that there was no substantial difference in photofrin uptake between noninduced HL60 cells, immature monocytes, immature neutrophils and cells differentiated along the eosinophilic pathway. In contrast, HL60 cells differentiated into macrophages (HL60 phi) exhibited markedly increased photofrin uptake, which was further enhanced by their pretreatment with bacterial lipopolysaccharide. Similar results were obtained with other photosensitizers tested: di- and tetrasulfonated aluminum phthalocyanines (A1PcS2 and A1PcS4), tetrasulfonated zinc phthalocyanine (ZnPcS4), tetraphenylporphine tetrasulfonate (TPPS4) and benzoporphyrin derivative monoacid (BPD). Despite marked differences in the state of self-aggregation and other chemical properties of these compounds, the degree of their preferential uptake by HL60 phi cells showed very little variation. In a typical experiment, the uptake of these photosensitizers by HL60 phi cells was four to five times higher than the uptake by noninduced HL60 cells. In addition to the fluorometric assay employed in most of the experiments, cellular concentration of A1PcS4 was determined by measurement of elementary aluminum using atomic absorption spectroscopy.
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PMID:The effect of differentiation on photosensitizer uptake by HL60 cells. 828 22

E-selectin, an endothelial-specific adhesion molecule best known for its role in leukocyte adhesion, is not detected in quiescent endothelial cells, but is induced by inflammatory stimuli. However, E-selectin is also expressed in proliferating endothelial cells under noninflammatory conditions in vivo and in vitro, suggesting that E-selectin is also regulated by growth signals. To investigate E-selectin expression in lipopolysaccharide-stimulated versus nonstimulated proliferating cells, we analyzed the distribution of E-selectin-positive human microvascular endothelial cells in G0/G1, S, and G2/M phases of the cell cycle under both conditions. Lipopolysaccharide treatment resulted in uniformly increased E-selectin expression in cells in G0/G1, S, and G2/M. In contrast, levels of E-selectin in nonstimulated proliferating cells showed a linear correlation with the percentage of cells in G2/M. E-selectin in proliferating endothelial cells was not reduced by addition of soluble tumor necrosis factor-alpha-receptor or soluble interleukin-1-receptor indicating that its expression was not due to endogenous production of either cytokine. In addition, E-selectin was increased in cells stimulated with basic fibroblast growth factor, a well-known mitogen for endothelial cells. E-selectin in proliferating endothelial cells is functional, as shown by E-selectin-dependent adhesion of the promyelocytic leukemia cell line HL-60 to subconfluent human microvascular endothelial cells. In summary, these studies indicate that E-selectin can be regulated by a non-inflammatory pathway that is related to the proliferative state of the endothelium.
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PMID:Noninflammatory expression of E-selectin is regulated by cell growth. 1033 84

Resveratrol (3,5,4'-trihydroxy-trans-stilbene) is a naturally occurring compound shown to inhibit carcinogen-induced preneoplastic lesion formation in mouse mammary organ culture and tumorigenesis in the two-stage mouse skin model. Cancer chemopreventive potential was also suggested in various assays reflective of the three major stages of carcinogenesis. Anti-initiation activity was indicated by its antioxidant and antimutagenic effects, inhibition of the hydroperoxidase function of cyclooxygenase (COX), and induction of phase II drug-metabolizing enzymes. Antipromotion activity was indicated by antiinflammatory effects, inhibition of production of arachidonic acid metabolites catalyzed by either COX-1 or COX-2, and chemical carcinogen-induced neoplastic transformation of mouse embryo fibroblasts. Antiprogression activity was demonstrated by its ability to induce human promyelocytic leukemia (HL-60) cell differentiation. Moreover, pretreatment of mouse skin with resveratrol significantly counteracted 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced oxidative stress, as evidenced by numerous biochemical responses. Resveratrol reduced the generation of hydrogen peroxide, and normalized levels of myeloperoxidase and oxidized-glutathione reductase activities. It also restored glutathione levels and superoxide dismutase activity. As judged by the reverse transcriptase-polymerase chain reaction, resveratrol selectively inhibited TPA-induced expression of c-fos and transforming growth factor-beta 1 (TGF-beta 1), but did not affect other TPA-induced gene products including COX-1, COX-2, c-myc, c-jun, and tumor necrosis factor-alpha. These data indicate that resveratrol may interfere with reactive oxidant pathways and/or modulate the expression of c-fos and TGF-beta 1 to inhibit tumorigenesis in mouse skin. As reported herein, in addition to the activities described above, resveratrol inhibited the de novo formation of inducible nitric oxide synthase (iNOS) in mouse macrophages stimulated with lipopolysaccharide. This finding suggests an additional mechanism by which resveratrol may function as a cancer chemopreventive agent.
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PMID:Cancer chemopreventive activity of resveratrol. 1037 Aug 67


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