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PubMed1989

The effects of 5-azacytidine, 12-O-tetradecanoylphorbol 13-acetate and sodium n-butyrate on reactivation of alphaherpesvirus saimiri from explant cultures of latently infected rabbit dorsal root ganglia.

The DNA hypomethylating agent 5-azacytidine greatly increased the reactivation of alphaherpesvirus saimiri-1 (alpha HVS) from latently infected rabbit dorsal root ganglia, although it inhibited the virus yield and plaque formation efficiency of alpha HVS in Vero cells. 12-O-Tetradecanoylphorbol 13-acetate (a protein kinase C activator) and sodium n-butyrate both had a stimulating action on replication in Vero cells but did not affect the release of alpha HVS from latently infected rabbit dorsal root ganglia.

Animals↗
PubMed1989

Sodium-N-butyrate induces cytoskeletal rearrangements and formation of cornified envelopes in cultured adult human keratinocytes.

The technique developed in our laboratory allows us to culture multilayered, stratified sheets of human keratinocytes, which can be used to cover the burn wounds of patients. Organization of cells in these cultures resembles stratum germinativum and stratum spinosum but there are only a few fully keratinized cells and the stratum corneum is not developed. Since the fully differentiated sheets may offer additional advantages as epidermal transplants, attempts were made to enhance the degree of differentiation in vitro. In the present study sodium-N-butyrate (NaB) was used as a differentiating agent and its effect on the cell cycle and cytoarchitecture of epidermal cells was investigated. Incubation of keratinocytes in the presence of 2.5 mM NaB induced the appearance of enucleated cornified envelopes, covering approximately 70-80% of the surface of the cultures. Their appearance correlated with a decrease in expression of keratin K13, previously shown to be inhibited during terminal differentiation of human keratinocytes. An increase in transglutaminase transferase activity was also observed. The induction of cornified layers also correlated with an increase in the amount of microfilament (MF)-associated actin. NaB also induced changes in the cell cycle distribution of the keratinocyte cultures. A decrease in the proportion of S and G1B phase cells was paralleled by an increase in G1A cells, maximally expressed 30-48 h following addition of the inducer. Interestingly, NaB also induced a cell arrest in G2 phase. These cell cycle perturbations preceded the onset of keratinocyte differentiation. The results indicate that the enhanced differentiation of human keratinocytes in the presence of NaB may serve as a means to produce epidermal sheets with improved properties for transplantation in a clinical setting. It also serves as an in vitro model system to study the interrelationships between biochemical events and cell cycle changes accompanying differentiation.

Butyrates↗
PubMed1993

The expression of human plasma cholesteryl-ester-transfer protein in HepG2 cells is induced by sodium butyrate. Quantification of low mRNA levels by polymerase chain reaction.

Although human plasma cholesteryl-ester-transfer protein (CETP) is primarily synthesized in the liver, its expression in a number of transformed liver cell lines is very low. However the use of the human hepatoma cell line HepG2 as a model system for the regulation of CETP on mRNA level is facilitated by a quantitative reverse-transcribed polymerase chain reaction. We demonstrate a time-dependent and concentration-dependent 3-4-fold induction of CETP mRNA by sodium butyrate. CETP mass in the medium is also augmented; however, the effect on protein level is less pronounced.

Base Sequence↗
PubMedDate not supplied

The ion exchange properties of human post-mortem caecal and colonic mucus: the effect of sodium butyrate.

This study examined Na+/H+ ion exchange of caecal and colonic mucus. Two distinct Na+/H+ ion exchange populations of caecal mucus were identified, one group being a cation exchanger and the other an anion exchanger, suggesting that caecal mucus has ampholyte properties responsive to changing physical and chemical properties of luminal contents. Mucus from the colon was consistently an anionic exchanger--this may aid water and electrolyte absorption in the colon. When mucus was incubated with sodium butyrate, the Na+/H+ ion exchange properties of the mucus were decreased.

Adolescent↗
PubMed1991

Retinoic acid inhibits sodium butyrate-induced monocytic differentiation of HL60 cells while synergistically inducing granulocytoid differentiation.

The human myeloid leukemia cell line HL60 is an in vitro model to study myeloid differentiation. HL60 cells differentiate along different cell type lineages in response to a variety of compounds. The direction of differentiation is usually inducer-specific. However, the response of HL60 cells to sodium n-butyrate (NaB) is pleiotropic. NaB induces HL60 along the monocytic, neutrophilic, eosinophilic, and basophilic pathways. In this study we saw that physiologic concentrations of all-trans-retinoic acid (RA) switched the direction of NaB-induced differentiation from monocytic to granulocytic. We showed previously (Breitman & He, Cancer Res 1990: 50: 6268-6273) that combinations of RA and NaB synergistically induce HL60 to cells that reduce nitroblue tetrazolium. The present study shows that this synergy was even greater if the parameter measured was mature granulocytes. Our results raise the possibility that the endogenous RA in the serum used to grow cells in culture may affect the direction of differentiation of HL60 cells induced by NaB. Furthermore, our results may provide additional rationale for the use of combinations of RA and NaB in the treatment of some leukemias.

Butyrates↗
PubMed1995

Shiga toxin-associated hemolytic uremic syndrome: effect of sodium butyrate on sensitivity of human umbilical vein endothelial cells to Shiga toxin.

Escherichia coli O157:H7-related vascular damage such as hemolytic uremic syndrome is believed to require the Shiga-like toxins. This study demonstrated that sodium butyrate sensitized human umbilical vein endothelial cells to Shiga toxin and increased the expression of Shiga toxin receptor, globotriaosylceramide (Gb3), on human umbilical vein endothelial cells.

Bacterial Toxins↗
PubMed1984

Epstein-Barr virus-specific DNase activity in nonproducer Raji cells after treatment with 12-o-tetradecanoylphorbol-13-acetate and sodium butyrate.

An Epstein-Barr virus (EBV)-specific DNase was induced in EBV nonproducer Raji cells after treatment with 12-O-tetradecanoylphorbol-13-acetate and sodium butyrate. The increase in EBV DNase activity was related to the appearance of early antigen-positive cells. The enzyme had a sedimentation coefficient of 4S and was resistant to 300 mM KCl, and its induction did not depend on viral DNA synthesis. The EBV-specific DNase activity was specifically inhibited by sera from patients who had nasopharyngeal carcinoma with high early antigen activities but not by sera from normal, healthy individuals. There was a correlation between the degree of anti-EBV DNase activity and the titers of early antigen antibody.

Antigen-Antibody Complex↗
PubMed1996

The herpes simplex virus type 1 latency-associated transcript promoter is activated through Ras and Raf by nerve growth factor and sodium butyrate in PC12 cells.

Herpes simplex virus establishes latent infections in the nuclei of sensory neurons. These infections are characterized by the abundant expression of a series of 5' coterminal transcripts termed the latency-associated transcripts (LATs). Available evidence indicates that LAT expression is specifically regulated in latently infected neurons. Although previous studies have examined the regulation of LAT expression in neuronal and nonneuronal cells, the mechanism of regulation of LAT expression in neuronal cells in response to external factors has not been investigated. To address this question, we characterized the activity of LAT promoter fusion constructs in PC12 cells following treatment with nerve growth factor (NGF) and/or sodium butyrate (NaB), agents that affect expression of cell cycle-associated genes. Expression from the LAT promoter was induced 8- to 12-fold by either NGF or NaB alone and 40- to 60-fold when the two agents were added simultaneously. Fibroblast growth factor also induced expression from the LAT promoter but to a lesser extent than NGF. Treatment with factors such as epidermal growth factor, phorbol myristate acetate, cyclic AMP, or KCI had no significant effect on LAT promoter activity. Notably, promoter-reporter constructs containing immediate-early (ICP0 and ICP4), early (ICP8 and UL9), and late (UL10 and UL30) viral promoters were induced only two- to fourfold by NGF, suggesting that the LAT promoter may be unusual among herpes simplex virus genes in the magnitude of its response to this factor. To identify pathways leading to LAT activation in vitro, we characterized the response of the LAT promoter to NGF and/or NaB in PC12-derived cell lines containing mutations in specific signal transduction pathways. We found that activation of the LAT promoter requires Ras activation and that activation of the serine/threonine kinase, Raf, is sufficient to induce LAT expression. Together, these results indicate that the LAT promoter is regulated via the Ras/Raf signal transduction pathway in response to external factors such as NGF and NaB and that LAT expression may be regulated by NGF in latently infected neurons.

Animals↗
PubMed1996

Identification of cis-acting sequences in the promoter of the herpes simplex virus type 1 latency-associated transcripts required for activation by nerve growth factor and sodium butyrate in PC12 cells.

In the absence of detectable viral proteins, expression of the latency-associated transcripts (LATs) is likely regulated by cellular factors during latent infection of neurons with herpes simplex virus type 1. The amounts and activation states of these factors may in turn be regulated by extracellular regulatory factors. Consistent with this hypothesis, we have recently demonstrated that LAT expression is significantly enhanced by nerve growth factor (NGF) and sodium butyrate (NaB) in neurally derived PC12 cells. With the ultimate goal of identifying trans-acting cellular factors involved in regulating LAT expression during latency, we have attempted to identify the cis-acting elements to which these putative cellular factors bind by characterizing the LAT promoter and a series of 5' promoter deletion mutants in PC12 cells following treatment with the LAT-enhancing agents NGF and NaB. Transient expression assays demonstrated that distinct cis-acting sequences mediate basal and induced LAT promoter expression. Basal activity in PC12 cells is mediated by two elements: a negative regulatory element between -435 and -270 and a positive element between -240 and -204. The positive element contains binding sites for the transactivator Sp-1, whereas the negative element bears some resemblance to known neuron-specific silencer elements. In contrast to basal expression, maximum induction of the LAT promoter by NGF and NaB requires sequences between -159 and -81. Using gel mobility shift assays, we have identified three sets of protein-DNA complexes that bind to this 78-bp region and shown by competition analysis that binding is specific. The abundance and mobility of these complexes were altered by treatment with NGF or NaB. The nucleotide sequences to which these complexes bind were fine mapped by competition analysis with oligonucleotide probes containing substitution mutations. The target sequences identified exhibit no homology to binding sites of known transcription factors. These regions were critical for complex formation in vitro and for maximum induction of the LAT promoter by NGF and NaB in transient expression assays. The protein complexes that form with target sequences likely participate in the regulation of LAT expression in response to physiological stimuli in neurons in vivo.

Animals↗
PubMed1983

Identification and characterization of Epstein-Barr virus-related surface polypeptides expressed on n-butyrate-treated P3HR-1 cells.

Seven polypeptides [300,000 (300K), 250K, 150K, 140K, 120K, 87K and 52K] were identified as Epstein-Barr virus(EBV)-related surface polypeptides expressed on n-butyrate-treated P3HR-1 cells. Five polypeptides (300K, 250K, 150K, 120K and 87K) were sensitive to phosphonoacetic acid, and four of these (300K, 250K, 120K and 87K) were glycoproteins. The 300K and 250K polypeptides had a slightly higher molecular size and the 87K polypeptide a slightly lower molecular size than the corresponding polypeptides detected in virus-producing P3HR-1 cells and in the envelope of EBV particles.

Antigens, Viral↗
PubMed1986

Plasminogen activator production from murine mastocytoma cells. Dissociation of plasminogen activator and histamine production by sodium butyrate.

Plasminogen activator (PA) production from mouse mastocytoma P815 was investigated. A trace level of PA was detected in the culture supernatant of P815, but addition of Con A (5 micrograms/ml) stimulated the PA production to the 20- to 50-fold of that of the unstimulated culture. Time course studies suggest that PA is actively synthesized and secreted during the culture period with Con A. Furthermore, pretreatment of P815 with sodium butyrate, which is known to differentiate interleukin-3-dependent bone marrow mast cells or P815 cells, increased the PA production from P815 cells in the presence or absence of Con A.

Animals↗
PubMed1987

Beige mouse mast cells generated in vitro: ultrastructural analysis of maturation induced by sodium butyrate and of IgE-mediated, antigen-dependent degranulation.

We derived growth factor-dependent mast cell lines from C57BL/6-bgJ/bgJ ('beige') mouse bone marrow cells using techniques previously described for deriving mast cell lines from normal mice. According to examination by transmission electron microscopy, the cytoplasmic granules of cultured mast cells derived from beige mice were larger in size and fewer in number than those in cultured mast cells derived from normal C57BL/6 mice. Mast cells derived from beige mice underwent maturation when exposed to sodium butyrate, as judged by increased content of electron-dense material in the cytoplasmic granules. Cultured mast cells derived from beige mice also underwent IgE-mediated, antigen-dependent anaphylactic degranulation which was similar in its ultrastructural features to that described for cultured mast cells from normal mice. However, in mast cells not stimulated with IgE and antigen, fusion between individual cytoplasmic granules was observed more commonly in mast cells derived from beige mice than in normal mast cells. This might mean that these events are more common in C57BL/6-bgJ/bgJ mast cells, and/or that their resolution is slower and thus more easily captured by electron microscopy.

Animals↗
PubMed1993

Effect of butyric acid on induction of differentiation into eosinophil-like cells in human eosinophilic leukemia cells, EoL-1 cell line: possible role of granulocyte-macrophage colony-stimulating factor as an autocrine differentiating factor.

EoL-1 cells differentiated into mature eosinophil-like cells when incubated with butyric acid (BA). The differentiated cells possessed many granules that stained with Luxol fast blue and acquired the ability to produce leukotriene C4 and eosinophil cationic protein (ECP), and migrated toward some eosinophillotactic attractants, including PAF, IL-5, IL-3 and GM-CSF. Monoclonal antibody to GM-CSF and IL-5, especially GM-CSF, strongly decreased the ability of BA to induce differentiation, whereas antibody to IL-3 did not. Recombinant human (rh) IL-3, rhGM-CSF and recombinant mouse (rm) IL-5, by themselves, did not have the ability to induce differentiation. On the other hand, the presence of these cytokines significantly (p < 0.01) augmented BA-induced cell differentiation. Other cytokines including rhIL-1 alpha/beta, rhIL-2, rhIL-4, rhIL-6, rhIL-8, rhTNF-alpha and rhIFN-gamma had no effect on differentiation. Expression of GM-CSF and GM-CSF receptor mRNA was detected in cellular RNA obtained from BA-stimulated EoL-1 cells. Moreover, about 5-10 pg/ml of GM-CSF was detected in the culture supernatant of BA-stimulated EoL-1 cells. These findings suggested that BA-induced EoL-1 cell differentiation was elicited under the influence of GM-CSF endogenously produced in these cells. GM-CSF also seemed to be an autocrine differentiating factor in EoL-1 cells.

Antibodies↗
PubMed1995

Sodium butyrate inhibits platelet-derived growth factor-induced proliferation of vascular smooth muscle cells.

Sodium butyrate (SB), a naturally occurring short-chain fatty acid, was investigated for its therapeutic value as an antiproliferative agent for vascular smooth muscle cells (SMCs). At 5-mmol/L concentration, SB had no significant effect on rat SMC proliferation. However, at the same concentration, SB inhibited platelet-derived growth factor (PDGF)-AA-, -AB-, and -BB-induced proliferation of SMCs. Exposure of SMCs to PDGF-BB resulted in activation of receptor intrinsic tyrosine kinase activity and autophosphorylation of beta-PDGF-receptor (beta-PDGFR). The activated beta-PDGFR physically associated and phosphorylated signaling molecules such as ras-GTPase activating protein (GAP) and phospholipase C gamma (PLC gamma). SB, in the absence of PDGF-BB, caused neither beta-PDGFR tyrosine phosphorylation nor phosphorylation and association of GAP and PLC gamma with beta-PDGFR. PDGF-BB-enhanced activation of receptor intrinsic tyrosine kinase activity and autophosphorylation of tyrosine residues of beta-PDGFR were unaffected by SB irrespective of whether SMCs were preincubated with SB before exposure to PDGF-BB plus SB or incubated concomitantly with PDGF-BB plus SB. Likewise, phosphorylation and association of GAP and PLC gamma with PDGF-BB-activated beta-PDGFR were unaffected. In addition, SB did not block PDGF-BB-stimulated, PLC gamma-mediated production of inositol triphosphate. Similarly, PDGF-BB-induced beta-PDGFR degradation was unaffected when SMCs were exposed to PDGF-BB plus SB, and SB by itself had no influence on beta-PDGFR degradation. Unlike beta-PDGFR kinase activity, mitogen-activated protein kinase (MAP-kinase) activity was stimulated by SB by about 2.7-fold. Exposure of SMCs to PDGF-BB caused an approximately 11.4-fold increase in MAP-kinase activity and this increase in activity was not significantly affected when cells were coincubated with PDGF-BB and SB (10.3-fold). However, pretreatment of SMCs with SB for 30 minutes and subsequent incubation in PDGF-BB plus SB abolished most of the PDGF-BB-induced MAP-kinase activity (4.6-fold). Transcription of growth response genes such as c-fos, c-jun, and c-myc were induced by PDGF-BB, and their induction was suppressed, particularly c-myc, by incubating SMCs with PDGF-BB plus SB. Similarly, preincubation of cells with SB for 30 minutes and subsequent incubation in PDGF-BB plus SB diminished PDGF-BB-induced transcription of c-fos, c-jun, and c-myc. However, SB by itself had no significant effect on c-fos, c-jun, and c-myc transcription.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2026

Intestinal organoid screen reveals that Bacillus velezensis PGM541 promotes epithelial proliferation via its metabolite butyric acid.

BACKGROUND: Probiotics have been widely used for the regulation of intestinal health. Current screening methods for probiotics typically rely on animal or two-dimensional cell models. In this study, we employed intestinal organoids to identify a candidate probiotic strain. Furthermore, we investigated the potential mechanisms through which this strain and its active metabolites exert their effects, thereby evaluating the efficacy of this screening approach. RESULTS: Firstly, candidate probiotic strain PGM541 was identified from a porcine-derived Bacillus library by assessing organoid viability. Subsequently, to validate the organoid screening reliability, the potential mechanism of strain PGM541 on the intestinal epithelium was investigated; it was found to exhibit probiotic functions by regulating cell proliferation in both in vitro organoid and in vivo piglet models. Furthermore, organoid screening combined with metabolomic analysis identified butyric acid (BA) as the key bioactive metabolite responsible for driving epithelial proliferation. Whole-genome and transcriptomic analyses revealed the biosynthetic pathway of BA in strain PGM541. Importantly, BA receptor blockade experiments directly confirmed that BA enhances epithelial proliferation via interaction with the FFAR2 receptor, thereby validating its functional activity. Additionally, strain PGM541 exhibited protective effects against dextran sulfate sodium (DSS)-induced colitis, further validating the effectiveness of the intestinal organoid platform for probiotic screening. CONCLUSIONS: The probiotic strain PGM541, which was screened using intestinal organoids, promotes intestinal epithelial cell proliferation via its metabolite BA activating the FFAR2 receptor. These findings demonstrate that the intestinal organoid model serves as an effective platform for both preliminary probiotic screening and mechanistic investigation. Video Abstract.

Animals↗
PubMed1992

Transcriptional regulation of prolactin receptor gene expression by sodium butyrate in MCF-7 human breast cancer cells.

The prolactin receptor (PRLR) mediates the diverse effects of prolactin, which in the mammary gland include the development of lobuloalveolar structures and increased tumor cell proliferation. Treatment of mammary carcinoma cells with the differentiating agent sodium butyrate (NaB) is known to reduce PRLR binding activity and PRLR gene expression, however the mechanism which mediates these changes is unknown, prompting this investigation. Using MCF-7 human breast cancer cells, assay of the rate of PRLR gene transcription by the nuclear run-on technique indicated that 3 mM NaB reduced PRLR gene transcription by 50% after 3 h of treatment and that this effect was maintained for at least 24 h. The protein synthesis inhibitor cycloheximide failed to abrogate this effect, which indicated that NaB did not require continuing protein synthesis to reduce the rate of PRLR transcription. Measurement of PRLR mRNA stability, using Northern blot analysis at various times after the inhibition of transcription with actinomycin D, showed that NaB treatment did not alter PRLR mRNA half-life. These results indicate that NaB inhibits PRLR gene expression by a transcriptional mechanism that does not require continuing protein synthesis.

Blotting, Northern↗
PubMed1995

Human fibroblasts (KMST-6/RAS cell line) transformed with 60Co gamma-rays and c-Ha-ras oncogene produce a large amount of granulocyte colony-stimulating factor (G-CSF); production is enhanced by cAMP, theophylline, and butyrate.

Human fibroblasts (KMST-6/RAS cell line), which was malignantly transformed in vitro with 60Co gamma-rays and the c-Ha-ras oncogene, produced a large amount of granulocyte colony-stimulating factor (G-CSF). The production was greater during the logarithmic growth phase than during the stationary phase. cAMP and theophylline, alone or in combination, and butyrate significantly enhanced G-CSF production, but dexamethasone or 5-azacytidine did not. Enhanced production of G-CSF by these agents was regulated at the posttranscriptional level. Neither the expression of the ras oncogene nor the tumorigenicity of the cells correlated with the production of G-CSF.

Butyrates↗
PubMed1992

Effect of dexamethasone, dimethylsulfoxide and sodium butyrate on a human hepatoma cell line PLC/PRF/5.

The effects of agents which are known to be differentiation inducers on a human hepatoma cell line PLC/PRF/5 were investigated. Dexamethasone (DEX), sodium butyrate (SB) or dimethylsulfoxide (DMSO) were examined. They all reduced cell proliferation but differ from each other in effect on the secretion of alphafetoprotein (AFP) and hepatitis B surface antigen (HBsAg), changes in morphology and RNA transcription. SB changed the cell from polygonal into a fibroblast-like type and decreased AFP secretion. DMSO decreased the cell size and changed AFP secretion in the same manner as SB. DEX changed the cell into a larger size, as well as increased AFP secretion. HBsAg secretion and also HB virus DNA transcription was enhanced by 3 agents. AFP and myc gene transcriptions were reduced by SB but DMSO reduced only AFP. Albumin gene transcription was enhanced by SB and DEX. These results indicate that the decrease of PLC/PRF/5 proliferation is induced through different mechanisms by these 3 agents.

Butyrates↗