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PubMed1993

The induction of jun genes during the reversible changes induced with sodium butyrate on the differentiation of F9 cells.

Sodium butyrate (NaB) induces the phenotypic changes and differentiation markers in embryonal carcinoma F9 cells (Kosaka et al., Exp. Cell Res. 192, 46, 1991). However, the effects are rapid and reversible and different from those induced with retinoic acid (RA). We examined the expression of jun genes during differentiation induced with NaB and compared it with that of RA induction. Although c-jun expression was induced with RA, rapid and predominant induction of junB expression was specifically observed with NaB, which is regulated by both transcriptional and post-transcriptional mechanisms. These results suggest that the mechanism of differentiation induced with NaB differs from that of RA; the former may be mediated by the junB gene and the latter by c-jun.

Animals↗
PubMed1995

Specialization switch in differentiating embryonic rat liver progenitor cells in response to sodium butyrate.

Embryonic (E) 12 rat liver epithelial cells constitute a population of bipotential progenitor cells which can differentiate along the hepatocyte (Hep) or biliary epithelial cell (BEC) lineage in primary culture. In the present study, E12 cells were seeded on fibronectin-coated substratum and exposed to sodium butyrate (SB) for various exposure times, and the emergence of the Hep or BEC phenotype was monitored by following the variations in albumin production and assessing the appearance of the two surface-exposed markers HES6 and BDS7. Continuous exposure to SB resulted into a major reduction in albumin production and, at Day 9 postseeding, few cells coexpressed BDS7 and albumin. When cells were exposed to SB for 5 days and then cultured for an additional 5 days without SB, they massively express BDS7, but very little HES6. Moreover, the reverse sequence, i.e., 5 days without SB followed by 5 days with it, led to the appearance of many cells expressing both HES6 and BDS7. These results indicate that progenitors committed preferentially along the Hep lineage still have the option to switch to BECs, at a transitional stage that we refer to as a "differentiation window."

Animals↗
PubMed1996

Differentiation of pancreatic carcinoma induced by retinoic acid or sodium butyrate: a morphological and molecular analysis of four cell lines.

The antiproliferative and differentiation-inducing effects of all-trans retinoic acid (RA) and sodium butyrate (SB) were investigated in four pancreatic ductal adenocarcinoma cell lines, two poorly differentiated ones (PT45 and PaTu-II), one moderately to poorly differentiated one (Panc-1) and one highly differentiated one (A818-1). Treatment with 20 microM RA resulted in moderate inhibition of cell growth in all cell lines, but clear evidence of cytodifferentiation (including elongated cell processes, increased rough endoplasmic reticulum, intensified immunostaining for the mucin marker (M1) was found only in PT45 and Panc-1. These phenotypic changes were paralleled by upregulation of RAR (retinoic acid receptor)-alpha and -gamma mRNA. SB (1 and 2 mM) treatment inhibited the cell growth of all cell lines much more prominently than RA. Cytodifferentiation was also largely restricted to PT45 and Panc-1. A noticeable phenomenon was enhancement of the expression of the neuroendocrine markers synaptophysin and Lcu7 in Panc-1 cells. In conclusion, it is evident that the original differentiation status of cells and their responsiveness to the agents are not clearly associated, and that RA responsiveness correlates with upregulation of RAR-alpha and -gamma mRNA.

Blotting, Northern↗
PubMed1988

Treatment with sodium butyrate inhibits the complete condensation of interphase chromatin.

The effects of histone hyperacetylation on chromatin fiber structure were studied using direct observations with the electron microscope. Histone hyperacetylation was induced in HeLa cells by treatment with sodium butyrate, and the ultrastructure of control and of acetylated chromatin fibers examined after fixation at different stages of compaction. No differences between control and acetylated chromatin were seen when the fibers were partially unfolded (10 mM NaCl, 20 mM NaCl, 50 mM NaCl), but in 100 mM NaCl, control chromatin showed further compaction to the "30 nm" fiber, while hyperacetylated chromatin failed to undergo this final compaction step. These results strongly suggest that histone acetylation causes a moderate "relaxation" rather than complete decondensation of interphase chromatin fibers. The relationship of these findings to the increased DNase I sensitivity of acetylated chromatin, and to transcription and replication, is discussed.

Acetylation↗
PubMed1991

The inhibitory action of sodium butyrate on the growth of KB, MMT and RPMI cells.

Three tumor cell lines (KB, MMT and RPMI) established from epithelial tissues were treated for 24 h with sodium butyrate (BU), the BU concentrations giving rise to 50% inhibition of [3H]thymidine incorporation were 2.0, 0.3, 0.2 mmol/L, respectively, for the KB, MMT and RPMI cell lines. Studies with [14C]BU have shown that, at similar degrees of inhibition of [3H]thymidine incorporation, the intracellular concentrations of BU are very close for all three cell types, despite the dissimilarity of the extracellular BU concentrations. These results imply that the BU sensitivity of the cells does not depend on the inhibition of thymidine incorporation, but on their BU uptake. The [3H]thymidine incorporation of MMT cells exposed to 5 mmol/L BU for 72 h returned to normal within the next 48 h. The same treatment accounted for about an 80-90% decrease in the cloning efficiency and tumourigenicity of MMT cells. These findings indicate that BU pretreatment inhibits DNA synthesis temporarily, while other parameters related to the cell growth, such as cloning efficiency and tumourigenicity, are durably influenced by BU pretreatment.

Animals↗
PubMed1989

Induction by sodium butyrate of cytomegalovirus replication in human endothelial cells.

Cultured endothelial cells are shown to be induced in regard to permissiveness to human cytomegalovirus by temporary treatment postinfection with sodium butyrate (1-2 mM). Drug-treated cells are demonstrated to exhibit expression of immediate early and early viral antigens, synthesis of viral DNA and viral structural glycoprotein B. Progeny virus could be visualized by electron microscopy.

Antigens, Viral↗
PubMed1994

Changes of antigen expression on human hepatoma cell lines caused by sodium butyrate, a differentiation inducer.

We have previously reported the effect of a differentiation inducer, sodium butyrate (SB), on human hepatocellular carcinoma (HCC) cell lines, demonstrating that it was a potent inducer of differentiation. In the present study, we investigated the alteration in expression of an antigen defined by a murine monoclonal antibody, H2, as well as alterations in the expression of other antigens, on the HCC cell lines HCC-T, HCC-M, and PLC/PRF/5, since it is known that specific antigenic changes occur during the differentiation of leukemic cells. The expression of the antigen defined by H2 increased immunocytochemically on HCC-T, HCC-M, and PLC/PRF/5 during treatment with SB. A flowcytometric study showed that almost all the HCC-T and HCC-M cells treated with SB highly expressed this antigen after 5 days' treatment. The antigen expression detected by H2 decreased after the removal of SB from the medium. On the other hand, antigen expression detected by another monoclonal antibody, 5C11, was not changed by this treatment. The expression of intracellular adhesion molecule (ICAM)-1 in HCC-T increased slightly, but that of beta 2-microglobulin and HLA-DR did not change. These results demonstrated that some antigen expression was changed by SB treatment and that the antigen defined by H2 seemed to be highly expressed on human HCC cells in the differentiated state.

Antibodies, Monoclonal↗
PubMed1992

Effects of butyrate homologues on metallothionein induction in rat primary hepatocyte cultures.

Sodium butyrate (NaB), a 4-carbon fatty acid, has been reported to activate the metallothionein (MT) gene in certain carcinoma cell lines. Because the effects of NaB are dependent on the cell type investigated, this study was conducted to determine if NaB and its homologues induce MT in rat primary hepatocyte cultures. Hepatocytes were grown on monolayer for 12 h and subsequently treated with formate, acetate, propionate (NaP), NaB, and valeric acid for 10 to 58 h. To examine their interaction with known MT inducers, cadmium (Cd), zinc (Zn), or dexamethasone (Dex) were added to some cultures. MT protein in the cells was quantitated by the Cd-hemoglobin assay; MT-1 mRNA was analyzed by Northern blot hybridizations with oligonucleotide probes, and quantitated by slot-blot analysis. Among the 1 to 5 carbon carboxylic acids, only NaP (3 carbon) and NaB (4 carbon) induced MT. NaP and NaB alone produced a moderate increase in MT two- to fourfold over control), but when combined with Cd or Dex, an additive increase was observed. However, when combined with Zn, a synergistic increase was detected. NaB and Zn synergistically increased MT protein, but produced only an additive increase in MT mRNA, suggesting the involvement of some posttranscriptional event(s) in the NaB-Zn induction of MT. In conclusion, NaP and NaB induced MT in normal cultured rat hepatocytes, producing an additive increase in MT protein with Cd and Dex, and a synergistic increase in MT protein with Zn.

Acetates↗
PubMed1990

Effects of 1,25-dihydroxyvitamin D3 and its analogs on butyrate-induced differentiation of HT-29 human colonic carcinoma cells and on the reversal of the differentiated phenotype.

1,25-Dihydroxyvitamin D3 (1,25-(OH)2D3) greatly enhances sodium butyrate (NaB)-induced enterocyte differentiation of HT-29 human colonic carcinoma cells while 1,25-(OH)2D3 alone induces growth restriction without associated differentiation. In the present study, the efficacies of various analogs of 1,25-(OH)2D3 to enhance NaB-induced HT-29 differentiation and to prolong the reversal of the differentiated phenotype under NaB-free growth conditions were subsequently examined. Extent of HT-29 differentiation was assessed by measurement of alkaline phosphatase (AP) activity, appearance of mucin-producing cells, changes in morphological characteristics, and expression of differentiation-associated cytokeratin proteins. Among active analogs of 1,25-(OH)2D3, 26,26,26,27,27,27-hexafluoro-1,25-(OH)2D3 (F6-1,25-(OH)2D3), 24,24-difluoro-24-homo-1,25-(OH)2D3, and 26,27-dimethyl-1,25-(OH)2D3 were 100-, 10-, and 5-fold, respectively, more effective than 1,25-(OH)2D3 in enhancing NaB-induced mucin production. Combined use of NaB and F6-1,25-(OH)2D3 (10(-9) M) also induced HT-29 cells to form highly differentiated goblet-like enterocytes, and increased both cellular AP enzymatic activity and tissue-type cytokeratin content. This differentiated state was qualitatively more advanced than that achieved by a combination of NaB and 10(-7) M 1,25-(OH)2D3. NaB-mediated HT-29 differentiation (in short-term inductions) was found to be reversible following a return to NaB-free medium. HT-29 cells differentiated by combined use of NaB and 1,25-(OH)2D3 or its analogs exhibited a significant prolonged reversal time relative to cells differentiated with NaB alone. The most prominent effect was achieved using cells differentiated with NaB and 10(-9) M F6-1,25-(OH)2D3 which exhibited a 7-fold prolonged reversal time over colonocytes differentiated by NaB alone. Our data suggest that a combined use of NaB and 1,25-(OH)2D3 or its derivatives may provide a convenient in vitro model system to probe molecular events associated with steroid-target tissue interactions in a differentiating cell system as commonly occurs in vivo. Such an analysis might lend itself to design of a rational combination differentiation-based therapy for the clinical management of colon cancer.

Butyrates↗
PubMed1988

n-Butyrate increases c-erb A oncogene expression in human colon fibroblasts.

We investigated the effect of n-butyrate (2.5 mM) on expression of the c-erb A oncogene in human colon fibroblasts. Exposure of these cells to the compound for 48 hours resulted in an increased accumulation of approximately 2.0 kb RNA which hybridized to a v-erb A cDNA probe. Hybridization to a beta-actin gene probe was unaffected by the treatment. This report is the first demonstration of a factor affecting expression of the c-erb A oncogene.

Actins↗
PubMed1992

Memory of butyrate induction by the Moloney murine sarcoma virus enhancer-promoter element.

We reported previously that a housekeeping gene could be converted to a butyrate-inducible gene by replacing its cognate promoter with the Moloney murine sarcoma virus enhancer-promoter element. In this study we report that the activated transcriptional state could be propagated from mother to daughter cells after the withdrawal of the inducer.

Adenine Phosphoribosyltransferase↗
PubMed1995

Sodium butyrate induces aberrant tau phosphorylation and programmed cell death in human neuroblastoma cells.

Paired helical filaments, one of the major hallmarks of Alzheimer's disease brains at autopsy, consist mainly of aberrantly phosphorylated tau. This aberrant tau phosphorylation can be induced in the human neuroblastoma cell line TR14 by a hyperstimulating mixture, consisting of nerve growth factor (NGF), db-cAMP, gangliosides and sodium butyrate (NaBut) [20,23]. Evidence is presented that exposing these cells to increasing concentrations of NaBut alone in the 0.5-2 mM dose-range is sufficient to induce aberrant tau phosphorylation within 24 h, measured by AT-8 immunocytochemistry and Western blotting. This process is associated with increased morphological differentiation. Furthermore, the aberrant tau phosphorylation is followed by neurotoxicity. This neurotoxicity has features of programmed cell death, such as fragmentation on a DNA agarose gel, fragmented nuclei and chromatin condensation and inhibition by the protein synthesis inhibitor cycloheximide. The mechanism by which NaBut induces these modified tau proteins and neurotoxicity are largely unknown but the data suggest an involvement of cytoskeletal proteins.

Antibodies, Monoclonal↗
PubMed1983

Interferon and sodium butyrate inhibit the stimulation of poly(ADP-ribose) synthetase in mouse cells stimulated to divide.

The activity of poly(ADP-ribose) synthetase, a chromatin-bound enzyme, increases when quiescent 3T3 cells are stimulated to proliferate. The elevation of enzymatic activity requires de novo RNA and protein synthesis. Interferon (IFN) or sodium butyrate, when added to quiescent cells at the time of stimulation, suppressed the rise of enzymatic activity as well as initiation of DNA synthesis in cells. However, other DNA synthesis inhibitors like methotrexate, FudR and hydroxyurea had little effect on the elevation of poly(ADP-ribose) synthetase in quiescent cells.

Animals↗
PubMed1986

Growth inhibition of murine melanoma by butyric acid and dimethylsulfoxide.

Treatment of B16-F10 melanoma cells with dimethylsulfoxide (DMSO) or butyric acid (BA) inhibits cell growth and delays tumor appearance in syngeneic mice. Both agents induce morphological changes in these cells. Treatment of melanoma cells with DMSO results in a marked increase in tyrosinase activity and melanin content. BA, on the other hand, does not increase melanin content and decreases tyrosinase activity. The data show that there are marked differences in the effect of DMSO and BA on melanin biosynthesis, whereas both agents inhibit cell growth and cause a delay in tumor appearance. These findings indicate that decreased proliferation of melanoma cells and induction of melanin biosynthesis are not necessarily associated phenomena.

Animals↗
PubMed1989

Thermal stability of nucleosomes studied in situ by flow cytometry: effect of ionic strength and n-butyrate.

Heating of cells permeabilized with ethanol and resuspended in aqueous media increases accessibility of DNA to intercalating dyes such as acridine orange (AO). The curves, representing increase in binding of AO as a function of rise in temperature, indicate that the transitions are cooperative. The transitions are sensitive to ionic strength and occur at lower temperatures when cells are suspended in media of increasing ionic strength. Extraction of histones raises accessibility of DNA to intercalators at room temperature, and heating has little effect on additional binding. The results are interpreted as indicating thermal destruction of nucleosomal structure in nuclear chromatin; dissociation of DNA from core histones results in its increasing ability to intercalate AO, most likely due to increased topological freedom to undergo unwinding and elongation following binding of the intercalator. Preincubation of cells with n-butyrate, known to induce histone hyperacetylation, lowers the heat stability of nucleosomes by about 5 degrees C. On the other hand, no differences are observed between chromatin of mitotic vs interphase cells tested over a wide range of ionic strengths (0.1-0.7 N NaCl). The method appears to be useful as a probe of chromatin structure at the nucleosomal level.

Acridine Orange↗
PubMed1990

TGF-alpha and TGF-beta expression during sodium-N-butyrate-induced differentiation of human keratinocytes: evidence for subpopulation-specific up-regulation of TGF-beta mRNA in suprabasal cells.

Sodium-N-butyrate (NaB) induces terminal differentiation and cornified envelope formation in cultured human keratinocytes. In the present study we explored the question of whether NaB-induced maturation could be mediated through changes in TGF-alpha and TGF-beta expression in normal keratinocytes. NaB induced a four-fold increase in TGF-beta mRNA transcript levels. This increase in TGF-beta mRNA abundance occurred only within the nonbasal keratinocyte subpopulation which maximally responds to NaB treatment by progression to cornified envelopes. Basal keratinocytes, which are relatively refractive to cornified envelope formation, did not show any increase in TGF-beta mRNA abundance after NaB treatment. By comparison, TGF-alpha mRNA transcript and extracellular TGF-alpha protein levels were unaffected by NaB treatment. A 50% decrease in EGF receptor binding was observed in NaB-treated keratinocyte cultures, rendering the cells less responsive to proliferation induction.

Butyrates↗
PubMed1992

Transforming growth factor-beta 1 acts cooperatively with sodium n-butyrate to induce differentiation of normal human keratinocytes.

Growth factors with established biological activity toward cultured normal human epidermal keratinocytes (NHEKs) (e.g., transforming growth factor-beta, TGF-beta; retinoic acid, RA) initiate programmed changes in cellular maturation which differ with regard to the specific differentiation pathway (normal or abnormal) analyzed. Sodium butyrate (NaB) initiates one form of epidermal differentiation leading to enhanced cornified envelope (CE) formation which involves abrogation of the normally inhibitory effect of RA on NHEK maturation. NaB also induces TGF-beta mRNA in the maturing suprabasal compartment, suggesting that TGF-beta may play a role in NaB-initiated NHEK differentiation. Treatment with TGF-beta 1 alone, however, only marginally increased (by twofold) the number of detergent-resistant CEs compared to control NHEKs and did not alter the prevalence of fully mature enucleated CEs. TGF-beta 1 was quite effective in inducing significant levels of CE expression when used simultaneously with suboptimal concentrations of NaB. The cooperative action of suboptimal NaB and TGF-beta 1 generated numbers of CEs which, in fact, exceeded the incidence of mature CEs formed in response to optimal levels of NaB alone. Neutralizing antibodies to TGF-beta, moreover, effectively reduced the incidence of CE formation in cultures treated with optimal NaB concentrations, further implicating endogenous TGF-beta activity in the NaB-initiated NHEK differentiation model. It is suggested, therefore, that within the NaB-induced pathway of NHEK differentiation, TGF-beta can positively modulate expression of the differentiated phenotype but alone is insufficient for generation of mature CEs.

Butyrates↗
PubMed1983

The effect of glutathione on HL-60 treated with dimethylsulfoxide, butyric acid or 12-O-tetradecanoylphorbol-13-acetate.

HL-60 promyelocytic leukemic cells can be induced to differentiate into granulocytes or macrophages. Reduced glutathione lyses undifferentiated HL-60 cells but has minimal effect on their differentiated counterparts. The addition of reduced glutathione to HL-60 promyelocytic leukemic cells retards cell growth and lyses cells. HL-60 cells can be induced to differentiate into granulocytes with dimethylsulfoxide butyric acid or into macrophages with 12-O-tetradecanoylphorbol-13-acetate. After treatment of HL-60 cells with these inducing agents the HL-60 cells become unresponsive to the effects of glutathione.

Butyrates↗