Effect of sodium butyrate on rumen epithelial cell proliferation
Ontology highlight
ABSTRACT:
ORGANISM(S): Ovis aries
PROVIDER: GSE252749 | GEO | 2024/04/03
REPOSITORIES: GEO
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Project description:Promoting rumen development is closely related to the health and efficient growth of ruminants. In the present study, we aimed to assess the impact of YAP1/TAZ on RE proliferation. The transcriptomic expression was analyzed to investigate the potential regulatory networks. The results indicated that GA promoted RE cell proliferation, while VP disrupted RE cell proliferation. The Hippo, Wnt, and calcium signaling pathways were altered in cells following the regulation of YAP1/TAZ. Upon YAP1/TAZ activation through GA, the CCN1/2 increased to promote RE cell proliferation. While when the YAP1/TAZ was inhibited by VP, the BIRC3 decreased to suppress RE cell proliferation. Thus, YAP1/TAZ may be potential targets for regulating RE cell proliferation. These findings broaden our understanding of the role of YAP1/TAZ and their regulators in RE and offer a potential target for promoting rumen development.
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Project description:Rumen epithelial parakeratosis, a common disease in ruminants caused by abnormalities in the ruminal stratified squamous epithelial keratinization process, negatively impacts ruminant health and performance. While we still lack a comprehensive perception of the underlying mechanisms and the predisposing factors for this disorder.Here, we investigated rumen epithelial cell heterogeneity, differentiation trajectories, and cornification to clarify the rumen epithelial keratinization process
2023-12-07 | GSE249083 | GEO
Project description:A healthy rumen is crucial for normal growth and improved production performance of ruminant animals. Rumen microbes participate in and regulate rumen epithelial function, and the diverse metabolites produced by rumen microbes are important participants in rumen microbe-host interactions. SCFAs, as metabolites of rumen microbes, have been widely studied, and propionate and butyrate have been proven to promote rumen epithelial cell proliferation. Succinate, as an intermediate metabolite in the citric acid cycle, is a final product in the metabolism of certain rumen microbes, and is also an intermediate product in the microbial synthesis pathway of propionate. However, its effect on rumen microbes and rumen epithelial function has not been studied. It is unclear whether succinate can stimulate rumen epithelial development. Therefore, in this experiment, Chinese Tan sheep were used as experimental animals to conduct a comprehensive analysis of the rumen microbiota community structure and rumen epithelial transcriptome, to explore the role of adding succinate to the diet in the interaction between the rumen microbiota and host.
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Project description:We performed global scale microarray analysis to identify detailed mechanisms by which sodium butyrate (SB) induce cell growth arrest and differentiation of colonic epithelial cells by using an Affymetrix GeneChip system. Colonic epithelial MCE301 cells used in this study were derived from transgenic mice harboring a tsSV40 large T-antigen. Arrested cell growth and a differentiated phenotype accompanying elevations of alkaline phosphatase activity and histone acetylation were observed in the cells treated with 2 mM SB. Of the 22,690 probe sets analyzed, approximately 2,000 genes were down- and up-regulated by a factor of 2.0 or greater in the cells treated with SB. Keywords: sodium butyrate, gene expression, colonic epithelial cell
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Project description:Machado-Joseph disease (MJD) is a fatal neurodegenerative disease caused by expansion of the trinucleotide repeat region within the ATXN3/MJD gene. Mutation of ATXN3 causes formation of neurotoxic ataxin-3 protein aggregates, neurodegeneration and motor deficits. Here we investigated the therapeutic potential and mechanistic activity of sodium butyrate (SB), the sodium salt of butyric acid, a metabolite naturally produced by gut microbiota, on cultured SH-SY5Y cells and transgenic zebrafish expressing human ataxin-3 containing 84 glutamine (Q) residues to model MJD. MJD SH-SY5Y cells were found to contain ataxin-3 oligomeric species and protein aggregates. Treatment with SB increased activity of the autophagy protein quality control pathway in the MJD cells, decreased presence of ataxin-3 aggregates and presence of ataxin-3 oligomers in an autophagy-dependent manner. Treatment with SB was also beneficial in vivo, improving swimming performance, increasing autophagy activity and decreasing presence of insoluble ataxin-3 protein species in the transgenic MJD zebrafish. Co-treating the MJD zebrafish with SB and chloroquine, an autophagy inhibitor, prevented the beneficial effects of SB on the zebrafish swimming, suggesting that the improved swimming performance was autophagy-dependent. To identify mechanism of the induction of autophagy by SB, we performed proteomic analysis of protein lysates from the SB treated and untreated MJD SH-SY5Y cells. We found that SB treatment had increased activity of Protein Kinase A and AMPK signaling. Immunoblot analysis confirmed that SB treatment had increased levels of acetylated FOXO1 protein. Further, co-treatment with an inhibitor of FOXO1 transcriptional activity (AS1842856) prevented the increase in autophagosome formation (LC3II/I) usually produced by SB treatment. Together our findings indicate that treatment with SB can increase activity of the autophagy pathway through a FOXO1-dependent process and that this has beneficial effects in vitro and in vivo. We propose that treatment with sodium butyrate warrants further investigation for the treatment of neurodegenerative diseases underpinned by proteinopathy mechanisms, including MJD.
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Project description:<p>Neonatal hypoxic-ischemic encephalopathy (HIE) refers to nervous system damage caused by perinatal hypoxia, which is the major cause of long-term neuro-developmental disorders in surviving infants. However, the mechanisms still require further investigation. In this study, we found that the butanoate metabolism pathway exhibited significantly decreased and short chain fatty acid (SCFAs)-producing bacteria, especially butyrate-producing bacteria, were significantly decreased in fecal of neonatal hypoxic-ischemic brain damage (HIBD) rats. Surprisingly, Sodium butyrate (SB) treatment could ameliorate pathological damage both in the cerebral cortex and hippocampus and facilitate recovery of SCFAs-producing bacteria related to metabolic pathways in neonatal HIBD rats. Moreover, we found that in samples from SB treatment neonatal HIBD rats cortex with high levels of butyrate acid along with aberrant key crotonyl-CoA-producing enzymes ACADS levels was observed compared HIBD rats. We also demonstrated that a decrease in histone 3-lysine 9-crotonylation (H3K9cr) downregulated expression of the HIE-related neurotrophic genes Bdnf, Gdnf, Cdnf and Manf in HIBD rats. Furthermore, SB restored H3K9cr binding to HIE-related neurotrophic genes. Collectively, our results indicate that SB contributes to ameliorate pathological of HIBD by altering gut microbiota and brain SCFAs levels subsequently affecting histone crotonylation-mediated neurotrophic-related genes expression. This may be a novel microbiological approach for preventing and treating HIE.</p><p><br></p><p><strong>Targeted SCFA brain metabolomics</strong> is reported in the current study <a href='https://www.ebi.ac.uk/metabolights/MTBLS4933' rel='noopener noreferrer' target='_blank'><strong>MTBLS4933</strong></a>.</p><p><strong>Untargeted fecal metabolomics</strong> is reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS4932' rel='noopener noreferrer' target='_blank'><strong>MTBLS4932</strong></a>.</p>
2022-10-12 | MTBLS4933 | MetaboLights
Project description:<p>Neonatal hypoxic-ischemic encephalopathy (HIE) refers to nervous system damage caused by perinatal hypoxia, which is the major cause of long-term neuro-developmental disorders in surviving infants. However, the mechanisms still require further investigation. In this study, we found that the butanoate metabolism pathway exhibited significantly decreased and short chain fatty acid (SCFAs)-producing bacteria, especially butyrate-producing bacteria, were significantly decreased in fecal of neonatal hypoxic-ischemic brain damage (HIBD) rats. Surprisingly, Sodium butyrate (SB) treatment could ameliorate pathological damage both in the cerebral cortex and hippocampus and facilitate recovery of SCFAs-producing bacteria related to metabolic pathways in neonatal HIBD rats. Moreover, we found that in samples from SB treatment neonatal HIBD rats cortex with high levels of butyrate acid along with aberrant key crotonyl-CoA-producing enzymes ACADS levels was observed compared HIBD rats. We also demonstrated that a decrease in histone 3-lysine 9-crotonylation (H3K9cr) downregulated expression of the HIE-related neurotrophic genes Bdnf, Gdnf, Cdnf and Manf in HIBD rats. Furthermore, SB restored H3K9cr binding to HIE-related neurotrophic genes. Collectively, our results indicate that SB contributes to ameliorate pathological of HIBD by altering gut microbiota and brain SCFAs levels subsequently affecting histone crotonylation-mediated neurotrophic-related genes expression. This may be a novel microbiological approach for preventing and treating HIE.</p><p><br></p><p><strong>Untargeted fecal metabolomics</strong> is reported in the current study <a href='https://www.ebi.ac.uk/metabolights/MTBLS4932' rel='noopener noreferrer' target='_blank'><strong>MTBLS4932</strong></a>.</p><p><strong>Targeted SCFA brain metabolomics</strong> is reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS4933' rel='noopener noreferrer' target='_blank'><strong>MTBLS4933</strong></a>.</p>
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Project description:This research explores the antiproliferative effects of short-chain fatty acid (SCFA) salts (magnesium acetate, sodium propionate, and sodium butyrate) on AGS gastric adenocarcinoma cells. Sodium butyrate (NaB) exhibited the most significant inhibitory impact. The study investigated synergistic interactions between NaB and the drug dexamethasone (Dex) using a combination index model. Dex and NaB at a 2:8 ratio showed strong synergy, surpassing mono treatments in inhibitory activity. NaB induced pro-oxidative effects, countered by Dex in combination. Cell population analyses indicated a shift towards apoptosis with Dex, NaB, and their combination. Proteomic analysis revealed downregulation of the oncogene TNS4, suggesting a potential mechanism for antiproliferative effects. These findings suggest NaB as a potential adjuvant therapy with Dex, prompting further exploration of combination therapies and molecular mechanisms, emphasizing the potential application of these postbiotics in gastric cancer treatment.
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2022-12-26 | GSE221507 | GEO
Project description:Alterations in the composition of the gut microbiome have an emerging role in brain function and behaviour. We have porposed that short chain fatty acids (SCFA) including propionate and butyrate which are present in the diet and are fermantation products of many gastrointestinal bacteria are contributing environmental factors in autism spectrum disorders (ASD). Here we used the microarray technology to compare global changes in gene expression profiles following exposure of PC12 cells to structurally related SCFA propionate and butyrate each in two different concentrations. Large number of affected genes, common for both SCFA were identified, including genetic networks and GO processes implicated in ASD. PC12 cells were exposed to propionate or butyrate. RNA was isolated from each experimental group (n=6, pooled samples) and subjected to genome-wide expression profiling using Affymetrix microarrays to reveal dose- and SCFA-specific changes in gene expression and specific molecular pathways or processes affected as compared to vehicle treated controls.
2014-06-02 | E-GEOD-56516 | biostudies-arrayexpress