Upregulation of AKR1C3 in Sodium Butyrate Treated G361 Cell.
Ontology highlight
ABSTRACT:
SUBMITTER: Lee YJ
PROVIDER: S-EPMC10733077 | biostudies-literature | 2023 Dec
REPOSITORIES: biostudies-literature
Publications
Upregulation of AKR1C3 in Sodium Butyrate Treated G361 Cell.
Lee Yoon Jin YJ Choi Yu Sung YS Kim Sooyoung S Heo Jae Young JY Kim Dong Sung DS Cho Moon Kyun MK
Annals of dermatology 20231201 6
Similar Datasets
Project description:As a histone deacetylase inhibitor, sodium butyrate involves in cellular events such as proliferation, differentiation,apoptosis and cell cycle control via reprogramming gene expression. However, the target genes associated with the cell cycle control and molecular signaling triggering cell apopotosis and death are not well elucidated.
2016-12-29 | GSE58571 | GEO
Project description:As a histone deacetylase inhibitor, sodium butyrate and its derivative sodium phenylbutyrate involve in cellular events such as proliferation, differentiation, apoptosis and cell cycle control via reprogramming gene expression. However, the gene associated with the cell cycle control and molecular signaling triggering cell apopotosis and death are not well elucidated. Here, we treated A549 cells,a cell line belong to the non-small cells lung cancer,with high concentration of sodium butyrate or sodium phenylbutyrate and then used microarray identified differentially-expressed mRNA during this process.
2017-06-10 | GSE86928 | GEO
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. MCE301 cells were treated with SB for 0, 6, 12 and 24 h. Total RNA samples were prepared from the cells. Gene expression was analyzed by a GeneChip® system with the Mouse Expression Array 430A which was spotted with 22,690 probe sets. Sample preparation for array hybridization was carried out as described in the manufactures instructions.
2007-12-07 | E-GEOD-4410 | biostudies-arrayexpress
Project description:The complication of type 2 diabetes (T2D) exacerbates brain infarction in acute ischemic stroke (AIS). Because butyrate-producing bacteria are decreased in T2D and butyrate has been reported to be associated with attenuated brain injury in AIS, we hypothesize that administering butyrate could ameliorate T2D-associated exacerbation of brain infarction in AIS. Therefore, we first validated that Chinese AIS patients with T2D comorbidity have significantly lower levels of fecal butyrate-producing bacteria and butyrate than AIS patients without T2D. Then, we performed a 4-week intervention in T2D mice receiving either sodium butyrate (SB) or sodium chloride (NaCl) and found that SB improved the diabetic phenotype, altered the gut microbiota, and ameliorated brain injury after stroke. Fecal samples were collected from T2D mice after SB or NaCl treatment and were transplanted into antibiotic-treated C57BL/6 mice. After 2 weeks of transplantation, the gut microbiota profile and butyrate level of recipient mice were tested, and then the recipient mice were subjected to ischemic stroke. Stroke mice that received gut microbiota from SB-treated mice had a smaller cerebral infarct volume than mice that received gut microbiota from NaCl-treated mice. This protection was also associated with improvements in gut barrier function, reduced serum levels of lipopolysaccharide (LPS), LPS binding protein (LBP), and proinflammatory cytokines, and improvements in the blood-brain barrier. IMPORTANCE Ischemic stroke is a major global health burden, and T2D is a well-known comorbidity that aggravates brain injury after ischemic stroke. However, the underlying mechanism by which T2D exacerbates stroke injury has not been completely elucidated. A large amount of evidence suggests that the gut microbiota composition affects stroke outcomes. Our results showed that the gut microbiota of T2D aggravated brain injury after ischemic stroke and could be modified by SB to afford neuroprotection against stroke injury. These findings suggest that supplementation with SB is a potential therapeutic strategy for T2D patients with ischemic stroke.
| S-EPMC8510264 | biostudies-literature
Project description:Glucagon-like peptide-1 (GLP-1) has a broad spectrum of biological activity by regulating metabolic processes via both the direct activation of the class B family of G protein-coupled receptors and indirect nonreceptor-mediated pathways. GLP-1 receptor (GLP-1R) agonists have significant therapeutic effects on non-alcoholic fatty liver disease (NAFLD) and steatohepatitis (NASH) in animal models. However, clinical studies indicated that GLP-1 treatment had little effect on hepatic steatosis in some NAFLD patients, suggesting that GLP-1 resistance may occur in these patients. It is well-known that the gut metabolite sodium butyrate (NaB) could promote GLP-1 secretion from intestinal L cells. However, it is unclear whether NaB improves hepatic GLP-1 responsiveness in NAFLD. In the current study, we showed that the serum GLP-1 levels of NAFLD patients were similar to those of normal controls, but hepatic GLP-1R expression was significantly downregulated in NAFLD patients. Similarly, in the NAFLD mouse model, mice fed with a high-fat diet showed reduced hepatic GLP-1R expression, which was reversed by NaB treatment and accompanied by markedly alleviated liver steatosis. In addition, NaB treatment also upregulated the hepatic p-AMPK/p-ACC and insulin receptor/insulin receptor substrate-1 expression levels. Furthermore, NaB-enhanced GLP-1R expression in HepG2 cells by inhibiting histone deacetylase-2 independent of GPR43/GPR109a. These results indicate that NaB is able to prevent the progression of NAFL to NASH via promoting hepatic GLP-1R expression. NaB is a GLP-1 sensitizer and represents a potential therapeutic adjuvant to prevent NAFL progression to NASH.
| S-EPMC6277380 | biostudies-literature
Project description:Promoting rumen development is closely related to the health and efficient growth of ruminants. We investigated the effect of sodium butyrate (SB) on rumen epithelium (RE), and whether the YAP1/TAZ-dependent alteration was involved in the RE developmental process induced by sodium butyrate. In the SB-treated cells, theYAP1/TAZ-dependent changes were not observed. SB increased the expression of genes involved in short-chain fatty acid (SCFA) metabolism, while YAP1/TAZ did not. Thus, SB mediated RE development was not associated with YAP1/TAZ.
2024-04-03 | GSE252749 | GEO
Project description:The liver plays a pivotal role in maintaining euglycemia. Biogenesis and function of mitochondria within hepatocytes are often the first to be damaged in a diabetic population, and restoring its function is recently believed to be a promising strategy on inhibiting the progression of diabetes. Previously, we demonstrated that the gut microbiota metabolite butyrate could reduce hyperglycemia and modulate the metabolism of glycogen in both db/db mice and HepG2 cells. To further explore the mechanism of butyrate in controlling energy metabolism, we investigated its influence and underlying mechanism on the biogenesis and function of mitochondria within high insulin-induced hepatocytes in this study. We found that butyrate significantly modulated the expression of 54 genes participating in mitochondrial energy metabolism by a PCR array kit, both the content of mitochondrial DNA and production of ATP were enhanced, expressions of histone deacetylases 3 and 4 were inhibited, beta-oxidation of fatty acids was increased, and oxidative stress damage was ameliorated at the same time. A mechanism study showed that expression of GPR43 and its downstream protein beta-arrestin2 was increased on butyrate administration and that activation of Akt was inhibited, while the AMPK-PGC-1alpha signaling pathway and expression of p-GSK3 were enhanced. In conclusion, we found in the present study that butyrate could significantly promote biogenesis and function of mitochondria under high insulin circumstances, and the GPR43-β-arrestin2-AMPK-PGC1-alpha signaling pathway contributed to these effects. Our present findings will bring new insight on the pivotal role of metabolites from microbiota on maintaining euglycemia in diabetic population.
| S-EPMC7382753 | biostudies-literature
Project description:Sodium butyrate and bufexamac treatment of activated CD4+ T cells impairs de novo HIV-1 infection. RNAseq was used to obtain information about the cellular changes upon treatment, which could explain the observed effects on HIV-1 infection
2021-03-11 | GSE146854 | GEO
Project description:In order to characterize alterations in cellular regulatory mechanisms associated with MDV reactivation, we employed microarray analysis to identify changes in gene expression in chemically-reactivated MDV transformed cell lines, specifically MSB1, RP2 and CU115. Differentially expressed genes identified in the MDV-transformed cell lines were then compared against differentially expressed genes in the REV-transformed CU91 cell line. This step was done to reduce the number of false positives (i.e. genes likely responding solely to sodium butyrate rather than MDV reactivation). Multiple cellular pathways are also affected by MDV reactivation, including those associated with apoptosis, the cell cycle, DNA repair, and immune response.
2018-08-23 | GSE103028 | GEO
Project description:Analysis of colorectal cancer (CRC) cell line HT-29 treated with Sodium Butyrate. Sodium Butyrate, a HDAC inhibitor present in gut, can differentiate the undifferentiated HT-29 to enterocytes by the induction of brush border enzyme alkaline phosphatase. Results provide the transcriptional profiling underlying the butyrate-induced differentiation of CRC.
2016-12-31 | GSE61429 | GEO