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PubMedDate not supplied

Effect of hexafluoro-1,25-dihydroxyvitamin D3 and sodium butyrate combination on differentiation and proliferation of HL-60 leukemia cells.

We have investigated the combined effects of 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] and its fluoroanalog 26,26,26,27,27,27-hexafluoro-1,25-(OH)2D3 [F6-1,25-(OH)2D3] with sodium butyrate (NaB) on growth and differentiation of HL-60 human promyelocytic leukemia cells. F6-1,25-(OH)2D3 was 10-fold more active than 1,25-(OH)2D3 for induction of cell differentiation in HL-60 cells. Exposure to suboptimal concentration of F6-1,25-(OH)2D3 and NaB had synergistic effects compared to that of F6-1,25-(OH)2D3 or NaB alone and in the presence of 0.1-0.3 mM NaB, the dosage of F6-1,25-(OH)2D3 required to inhibit cell growth and colony formation and to induce cell differentiation was significantly reduced. The mechanism for the synergistic effect is probably that NaB increases cytoplasm content and nuclear binding of 1,25-(OH)2D3.

Antigens, CD↗
PubMed1992

Hydroxyurea-induced HbF production in anemic primates: augmentation by erythropoietin, hematopoietic growth factors, and sodium butyrate.

Hydroxyurea, a cell-cycle-specific cytotoxic agent, has been shown to increase fetal hemoglobin (HbF) production. This property makes it an attractive drug for treatment of sickle cell disease and severe beta thalassemia. Its potential efficacy is limited because of a variable and often suboptimal response. Combinations of hydroxyurea and other drugs may induce more clinically significant increases in HbF. We have utilized chronically phlebotomized rhesus monkeys, treated with oral hydroxyurea, to investigate the capacity of several other agents to further augment HbF synthesis. Recombinant human erythropoietin, in super-pharmacologic doses, increased F-reticulocyte production when given on a weekly sequential schedule (3 of 7 days) with hydroxyurea (4 of 7 days), but it was less effective on an alternate day schedule when hydroxyurea was given daily. Neither recombinant human interleukin 3 (IL-3) nor recombinant human granulocyte-macrophage colony-stimulating factor (GM-CSF), when infused individually, increased F-reticulocytes in animals receiving daily hydroxyurea. Sequential, overlapping infusions of IL-3 and GM-CSF produced a small but statistically significant increase in F-reticulocytes in one of two hydroxyurea-treated animals. Infusions of sodium butyrate produced a substantial augmentation in F-reticulocyte production in animals chronically treated with hydroxyurea. Thus, our studies have identified several agents that may prove useful in combination with hydroxyurea to achieve clinically beneficial levels of HbF.

Administration, Oral↗
PubMed1991

Up-regulation of delta opioid receptors in neuroblastoma hybrid cells: evidence for differences in the mechanisms of action of sodium butyrate and naltrexone.

Opioid binding in subcellular fractions from neurohybrid cells was assessed using two models of up-regulation. Homologous up-regulation was achieved by treating NG108-15 cells with the opioid antagonist naltrexone. Na butyrate was added to NCB-20 cell cultures to affect heterologous up-regulation. In both paradigms light and heavy membranes were resolved by concanavalin A (con A) pretreatment of cells followed by density centrifugation. [3H][D-Ala2,D-Leu5]enkephalin (DADLE) and [3H]diprenorphine Bmax values for these fractions increased without changes in affinity. In contrast to 48 h of antagonist treatment, 5 min of exposure to naltrexone down-regulated heavy membrane delta sites. Under both conditions of up-regulation, inhibition of LM [3H]DADLE specific binding by 5'-guanylylimidodiphosphate was enhanced suggesting greater receptor coupling to guanine nucleotide binding regulatory proteins. Although attenuated by addition of cycloheximide, [3H]DADLE binding to total homogenates increased upon naltrexone treatment of NG108-15 cells. Heavy membrane Bmax values were also augmented in the presence of cycloheximide and naltrexone for 48 h. Activities of beta-glucuronidase and beta-hexoseaminidase were diminished in total homogenates and subcellular fractions from naltrexone-treated cells, suggesting an opioid-induced alteration in lysosomal enzyme trafficking. Comparable receptor down- and up-regulation and attenuation of lysosomal enzyme activity were elicited by the delta-selective opioid peptide antagonist (allyl)2 Tyr-Aib-Aib-Phe-Leu-OH. These results suggest that homologous up-regulation entails initial down-regulation and blockade of receptor degradation.

Binding Sites↗
PubMed1990

Effect of liposomes containing sodium butyrate conjugated with anti-CD19 monoclonal antibody on in vitro and in vivo growth of malignant lymphoma.

A differentiation-inducer, sodium butyrate (SB), encapsulated in liposomes conjugated covalently to a monoclonal antibody directed to CD19 antigen, was successfully targeted to human lymphoma cell lines SKLY-18 and Ramos grown in vitro and in vivo in nude mice. Various control liposomes (lacking SB, lacking antibody, containing SB alone, or coupled to irrelevant antibody) were not effective targeters. Growth of tumor cells not expressing the relevant antigen was unaffected by the antibody-SB-liposome complex. Suppression of lymphoma growth in vivo was remarkable, and tumor regression was observed under certain conditions, although changes in morphology were not clearly observed. In view of the practical nonexistence of "tumor-specific" antigens, targeting of differentiation-inducers or growth modifiers, rather than cytotoxic drugs, to tumor cells, as exemplified in these experiments, may provide a useful approach for conversion of highly malignant to less malignant tumors, although the exact mechanism of the growth inhibitory effect on B-cell lymphoma of the anti-CD19 antibody-SB-liposome complex is unknown.

Animals↗
PubMed1991

Effects of sodium butyrate on proliferation-dependent insulin gene expression and insulin release in glucose-sensitive RIN-5AH cells.

A rat islet tumor subclone, RIN-5AH-T2-B, was cultured with 2 mmol/liter of the proliferation-arresting compound sodium butyrate (NaB). Insulin gene expression and glucose-stimulated insulin release were analyzed and compared with logarithmically proliferating and confluent control cells cultured without NaB. Logarithmically proliferating control cells revealed high insulin gene expression. In the presence of amino acids, these cells showed a dose-dependent insulin response to glucose with a half-maximal and maximal 6.5-fold stimulation by 0.8 and 5.6 mmol/liter D-glucose, respectively. However, as the control cells approached growth arrest, insulin gene expression subsided to below detectability, an occurrence that is associated with decreased insulin release and accumulation of cells in the G1 phase of the cell cycle. In contrast, NaB-arrested cells showed continuous insulin gene expression throughout the experiment. Despite this, insulin release in response to glucose was lost. NaB revealed a biphasic effect on the cell-cycle: after an initial leaky G1 arrest during the first 24 h, the 5AH-B cells were arrested in G2 during the following 3 days. These data suggest that insulin gene expression and glucose-stimulated insulin release are affected by the cell cycle. These glucose-sensitive RIN-5AH-T2-B cells may be useful in studies of insulin secretion and gene regulation.

Animals↗
PubMed1991

[The effects of sodium butyrate (NABT) on fibrillar centres and Ag-staining protein of nucleolus of human stomach glandular carcinoma (MGC-803) cells].

The changes in the ultrastructure of fibrillar centres, morphological type of nucleolus, and the content of Ag-nucleolus protein of Sodium Butyrate treated MGC-803 cells have been studied. It was found that the number of fibrillar centres and Ag-staining granules, content of Ag-staining protein of nucleolus were decreased, and nucleolar morphological type was changed from reticulated to ring-shaped in NaBT treated MGC-803 cells. These results indicate that NaBT regulate the proliferation and differentiation of cells by inhibiting rRNA synthesis and rDNA transcriptional activity.

Adenocarcinoma↗
PubMed1991

Induction of dormant HIV-1 by sodium butyrate: involvement of the TATA box in the activation of the HIV-1 promoter.

Reactivation of latent HIV-1 is believed to play a major role in the pathogenesis of AIDS. Here we show that sodium butyrate (NaB), which can cause gene induction or cell differentiation, reactivates dormant HIV-1 in vitro in chronically infected cells of T-lymphoid and monocytoid origin. The effect of NaB on HIV-1 expression in T-lymphoid cells was apparent 3 h after addition of drug and peaked at 24 h. During this time the proportion of HIV-1 antigen expressing cells increased from less than 0.5 to greater than 90%, and virus production increased by three orders of magnitude. The virus released by the NaB-induced cells was infectious. The extent and kinetics of NaB effects were similar to effects of phorbol 12-myristate 13-acetate in T cells, but not monocytes. Transient expression assays using an indicator gene under the control of the HIV-1 long terminal repeat revealed that mutations which altered the nucleotide sequence in the TATA box significantly reduced the NaB effect. These data show that NaB is a potent inducer of dormant HIV-1 and suggest that the TATA motif is required for this activity.

Butyrates↗
PubMed1991

[Effect of sodium butyrate on chromosome number and DNA content of human gastric adenocarcinoma cell line].

After treatment with n-sodium butyrate for 7 days, the inhibition of growth rate of human gastric adenocarcinoma cell (MGc 80-3) in culture reaches 50.7%. About 90% of the cancer cells treated with the drug undergo obvious differentiation, and their ultrastructure is also changed. Moreover, the cancer cells which have hyperdiploid chromosomes increase from 78% to 96%; on the contrary, the percentage of hypertriploid cells decreases from 6% to 2%, while that of hypertetraploid cells diminishes from 14% to 2%. By using the combination of 3H-TdR autoradiography and Feulgen cytophotometry to measure the cellular DNA content of unlabelled cells (G1), it is shown that the DNA amount in the experimental group is lower than that in the control group. Furthermore, the DNA content of undifferentiated cells in the unlabelled cells (G1) of the experimental group is hyperhexaploid in amount (D1 = 3.76 and 3.56), and about 90% undifferentiated cells have a DNA value of over 6 C. On the other hand, the differentiated cells in the unlabelled cells on the above same slide have near-tetraploid DNA values (D1 = 2.03 and 1.99), and a DNA content below 4 C is found in about 60% differentiated cells. The difference in DNA amount between these two categories of cells is statistically significant. The results mentioned above suggest that although the amount of genetic material in the morphologically differentiated cells has markedly decreased, these cells still do not represent normal diploid cells.

Adenocarcinoma↗
PubMed1991

Effect of butyrate and corticosteroids on retinoblastoma in vitro and in vivo.

The effect of sodium butyrate (NaB) alone and in combination with a glucocorticoid was studied on Y-79 retinoblastoma cells both in vitro and in vivo. Both NaB (0.5 and 4 mM) and hydrocortisone (1-100 microM) added separately to cells grown in suspension resulted in a small growth inhibition (less than 15%). A marked synergistic effect (75-77% growth inhibition) was observed in vitro when NaB and hydrocortisone were added in combination at all the concentrations tested. With in vivo experiments using the nude mouse model of retinoblastoma, the combination of NaB and methylprednisolone did not inhibit tumor growth.

Animals↗
PubMed1990

Retinoids and butyrate modulate fibroblast growth and contraction of collagen matrices.

Wound healing in the eye may lead to undesirable sequelae such as proliferative vitreoretinopathy and scarring of glaucoma filtering fistulas. We therefore sought to manipulate in vitro two key wound healing processes--cell proliferation and contraction of extracellular matrices--using vitamin A (VA), retinoic acid (RA), and n-butyrate (BUT). These substances modulate growth and differentiation of normal and neoplastic cells. We examined the effects of these agents on cultured rabbit fibroblast proliferation and contraction of collagen matrices. Dermal fibroblast proliferation was unaffected by VA, stimulated by RA, and inhibited by BUT. Scleral fibroblast proliferation, in contrast, was stimulated by both VA and RA. All three agents mildly inhibited fibroblast contraction of collagen matrices. We conclude that 1) VA, RA, and BUT have differential effects on rabbit fibroblast proliferation; 2) retinoid effects on fibroblast growth vary with the tissue of origin; and 3) VA, RA, and BUT modestly inhibit fibroblast contraction of extracellular matrices. This study suggests that fibroblast-mediated processes in ocular wound healing and cicatricial disease may be differentially modulated by retinoids and BUT.

Analysis of Variance↗
PubMedDate not supplied

Regulation of distribution, amount and ligand affinity of sugar receptors in human colon carcinoma cells by treatment with sodium butyrate, retinoic acid and phorbol ester.

Human colon carcinoma cells were treated with non-toxic levels of sodium butyrate, retinoic acid or phorbol ester, eliciting characteristic growth inhibition and morphological changes. Since protein-carbohydrate interactions are supposedly involved in regulatory processes and can serve within targeted drug delivery, the capacity to bind components of the carbohydrate chains of cellular glycoconjugates was monitored for such cells in relation to the type of the medium additive. The pattern of binding of a panel of neoglycoproteins was significantly altered for fixed cells, depending on the type of putative maturation factor. Quantitation of cell surface sugar receptors at a non-saturating concentration of neoglycoenzyme, employed as carbohydrate ligand-exposing probe, led to a similar conclusion. Up to six-fold increases were determined for individual probes. Binding studies with varying concentrations of neoglycoenzymes in the case of four ligands revealed that the receptor density, but not the affinity was significantly affected. Biochemical analyses corroborated this result by demonstrating mainly quantitative differences after affinity chromatography of detergent extracts from the four types of cell pellet. By showing the inhibitory potency of neoglycoprotein-conjugated liposomes in the cell binding assay with neoglycoenzymes, a perspective is indicated, of how the different effects of the differentiation-inducing agents might be beneficially exploited in targeted drug delivery.

Adenocarcinoma↗
PubMed1990

Combinations of retinoic acid with either sodium butyrate, dimethyl sulfoxide, or hexamethylene bisacetamide synergistically induce differentiation of the human myeloid leukemia cell line HL60.

All-trans-retinoic acid (RA), sodium n-butyrate (NaB), hexamethylene bisacetamide (HMBA), and dimethyl sulfoxide (DMSO) induce differentiation of the human acute myeloid leukemia cell line HL60. In the clinic, RA, NaB, or HMBA induce complete or partial remissions. However, the achievement and maintenance of effective plasma concentrations and toxicity have been problems. These difficulties led us to study the interaction of RA with these inducers. We found that combinations of RA with either NaB, HMBA, or DMSO synergistically induced terminal differentiation of HL60. A measure of the effectiveness of these combinations was that the doses of NaB, HMBA, and DMSO required alone to induce half-maximal differentiation were decreased about 4-fold in combination with normal plasma concentrations of about 30 nM RA. RA or NaB alone did not enhance the growth of HL60 cells. In contrast, HMBA or DMSO alone increased growth of HL60 cells even at concentrations that did not induce differentiation. The addition of RA reduced the promotion of growth and increased the extent of terminal differentiation seen with HMBA and DMSO alone. These data suggest that treatment of some malignancies with combinations of RA with HMBA or NaB may maintain differentiation-inducing effects and decrease the problems associated with the achievement and maintenance of effective plasma concentrations as single agents.

Acetamides↗
PubMed1989

Sodium butyrate-induced structural and functional modifications in proteins of cultured rabbit articular chondrocytes.

The effects of sodium butyrate (NaB), a potent growth inhibitory agent, on actin distribution, alkaline phosphatase (AP) activity and protein content were studied in rabbit articular chondrocytes in monolayer culture. When growth of randomly proliferating cells was arrested with NaB, actin stress fibers appeared; at the same time, vimentin-containing intermediate filaments and tubulin-containing microtubules were dispersed. Concomitantly, membrane AP activity and protein content were increased. Such effects support the hypothesis that NaB affects the expression of many proteins by modification of gene expression, probably at the transcriptional level.

Alkaline Phosphatase↗
PubMed1989

[Studies on cell surface fibronectin of transformed Syrian hamster lung cells induced by butyric acid].

In this paper, Fn was analysed qualitatively and quantitatively in three Syrian hamster cell lines, ie, nontransformed baby hamster lung fibroblasts cell line (BHL), a transformed cell line (BHLB4) and a butyric acid-induced phenotypically reversed cell line (ButB4) respectively. Fn was visualized on cell surface by means of indirect immunofluorescence technique. Immunofluorescence of Fn on the surface of BHL was bright with a stripe-like distribution, while that on the surface of BHLB4 was very dim or dispersed. On ButB4 cell surface, the intensity and distribution of immunofluorescence was similar to that on BHLB4 cells. Fn was isolated by affinity chromatography from the cell surface of the three cell lines. Its molecular weight was 250 kDa on SDS-polyacrylamide electrophoresis. The quantity of Fn isolated from surface of ButB4 was a bit lower than that from BHL, but was much higher than that from BHLB4. The result offers us a useful criterion for transformation and reverse transformation.

Animals↗
PubMed1986

Effects of sodium butyrate and dibutyryl cyclic AMP on thermosensitivity of HeLa cells and their production of heat shock proteins.

When HeLa cells were incubated at 42 degrees C for 6 h with 1 mM sodium butyrate or when cells treated with 1 mM dibutyryl cyclic AMP for 24 h were incubated at 42 degrees C for 6 h, they were more thermoresistant than heated control cells without such drugs. The production of heat shock proteins was not enhanced by the drug treatment. These results suggest that there is a factor (or factors) other than heat shock proteins that accounts for the thermoresistance of HeLa cells.

Bucladesine↗
PubMed1987

Induction of virus enzymes by phorbol esters and n-butyrate in Epstein-Barr virus genome-carrying Raji cells.

Phorbol esters and n-butyrate (SB) together could induce Epstein-Barr virus (EBV) DNA polymerase and DNase activities in Raji cells (virus nonproducer). Neither 12-O-tetradecanoylphorbol-13-acetate (TPA) nor SB alone could induce these EBV enzyme activities, transcription of the EcoRI C-region or other EBV proteins in Raji cells. The enzyme induction caused by exposure of Raji cells to TPA-SB was the result of the synthesis of virus-specified RNA, and the increase of linear EBV DNA content in Raji cells caused by TPA alone was not sufficient for induction of EBV-enzyme activities. Temporal characteristics of the TPA-SB induction process, but not the phorbol 12,13-dibutyrate-SB induction process, in Raji cells were observed; a critical phase (10-24 h) postphorbol ester treatment in phorbol 12,13-dibutyrate-SB-treated Raji cells which was responsible for the synthesis of virus RNA and enzymes was found. Phospholipase C, which increases intracellular diacylglycerols (and subsequently activates protein kinase C) was able to partially substitute for TPA in the TPA-SB induction for EBV polymerase and DNase activities. Sphingosine, a protein kinase C inhibitor, partially prevented the induction of virus enzyme activities in Raji cells treated with phorbol 12,13-dibutyrate and SB. No apparent changes in the methylation state of EBV DNA (EcoRI C region) were observed when Raji cells were treated with SB and TPA, alone or in combination. These results suggest that induction of EBV polymerase and DNase activities by TPA-SB may involve protein kinase C activation and another factor triggered by SB which together increase transcription of EBV DNA.

Burkitt Lymphoma↗
PubMed1986

Interferon and butyrate treatment leads to a decreased sensitivity of NK target cells to lysis by homologous but not by heterologous effector cells.

Human K-562 and HHMS cells were pretreated with human recombinant interferon (IFN)-gamma and used as targets in NK assays against human and murine effector cells. A protective effect against NK lysis was observed only in the homologous assay, whereas no change or even a slight increase in NK sensitivity against heterologous effector cells was found. In cold target inhibition experiments IFN-treatment of K-562 cells led to a decrease in their capacity to act as competitors in the homologous NK assay, leaving their inhibitory capacity unaltered in the heterologous assay. In accordance with results observed using human NK targets, murine YAC-1 cells treated with mouse recombinant IFN-gamma did not lose their susceptibility to human NK cells. However, they were markedly less susceptible to lysis mediated by murine effectors. Butyrate, another compound causing decreased sensitivity of K-562 cells for human natural killing, also failed to reduce the susceptibility against murine NK cells. The results indicate that the NK-resistant tumor target phenotype caused by IFN or differentiation-inducing agents can only be detected by homologous but not by heterologous effector cells. This suggests that major differences exist between the inter- and intraspecies NK killing mechanisms.

Animals↗