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Riboflavin depletion impairs cell proliferation in intestinal cells: Identification of mechanisms and consequences

ABSTRACT: Microarray analysis has been applied to the cell proliferation in a human colonic cel line, Caco-2. We have shown previously that a moderate riboflavin depletion around weaning has a profound impact on the structure and function of the small intestine of the rat, which is not reversible following riboflavin repletion. In this study we have modelled riboflavin deficiency in a human cell line, shown irreversible loss of cell viability associated with impaired mitosis and identified candidate effectors of riboflavin depletion in the cell. The aim of the present study is to develop a cell culture model of riboflavin depletion and analyse its behaviour using a using a combination of cell biology approaches including microarray analysis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE15132 | GEO | 2009/03/06

SECONDARY ACCESSION(S): PRJNA114951

REPOSITORIES: GEO

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Riboflavin depletion impairs cell proliferation in intestinal cells: Identification of mechanisms and consequences

Project description:Microarray analysis has been applied to the cell proliferation in a human colonic cel line, Caco-2. We have shown previously that a moderate riboflavin depletion around weaning has a profound impact on the structure and function of the small intestine of the rat, which is not reversible following riboflavin repletion. In this study we have modelled riboflavin deficiency in a human cell line, shown irreversible loss of cell viability associated with impaired mitosis and identified candidate effectors of riboflavin depletion in the cell. The aim of the present study is to develop a cell culture model of riboflavin depletion and analyse its behaviour using a using a combination of cell biology approaches including microarray analysis. A human colonic cell line, Caco-2, was grown in culture and treated to riboflavin depletion. Treated and untreated cells were collected at appropriate time points and isolated RNA subjected to microarray analysis.

2009-03-06 | E-GEOD-15132 | biostudies-arrayexpress

Riboflavin depletion regulates cell proliferation and cell cycle progression‑associated genes in HEK293T cells

Project description:Transcriptome analysis of RNA samples from riboflavin-depleted HEK293T cells. Riboflavin is an essential component of the human diet and its derivative cofactors have an established role in oxidative metabolism. Riboflavin deficiency has been linked with various human diseases. In this study, we have modelled riboflavin deficiency in HEK293T cell line, shown remarkable increase of cell proliferation. The aim of the present study is to develop a cell culture model of riboflavin depletion and analyze its molecular mechanism of acceleration cell proliferation. So, we used Affymetrix Human Transcriptome Array 2.0 to identify genes that were differentially expressed upon riboflavin-depleted HEK293T cells.

2017-05-16 | GSE98927 | GEO

Transcriptomics and Real-Time PCR analysis reveals a cross-modulatory effect between riboflavin and iron and outlines common and specific responses to riboflavin biosynthesis and uptake in Vibrio cholerae

Project description:Riboflavin-derived molecules such as flavin mononucleotide and flavin adenine dinucleotide comprise the most important redox coenzymes all across life kingdoms. Vibrio cholerae, a pandemic diarrheagenic bacterium, is able to synthesize riboflavin through the riboflavin biosynthetic pathway (RBP) and to internalize exogenous riboflavin using the RibN importer. This bacterium thrives in different environments such as estuarine waters and the human intestinal tract. The presence of two independent riboflavin supply pathways in this species may be related to the variable riboflavin availability and requirements across different niches. In order to gain insights into the role of the riboflavin provision pathways in the physiology of V. cholerae, we analyzed the bacterial transcriptomics response to extracellular riboflavin and to the deletions of ribD (RBP-deficient strain) or ribN. Notably, many genes responding to riboflavin have been previously reported to belong to the iron regulon. Real time PCR analysis confirmed this effect and further documented that reciprocally, iron regulates RBP and ribN genes in a riboflavin-dependent way. A subset of genes were responding to both ribD and ribN deletions. Nonetheless, a group of genes was specifically affected in the ∆ribD strain, on which the functional terms protein folding and oxidation reduction process were enriched. Also, a subset of genes was affected specifically in the ∆ribN strain, on which the cytochrome complex assembly functional term was enriched. Results indicate that iron and riboflavin interrelate to regulate its respective provision genes and suggest that both common and specific effects of biosynthesized and internalized riboflavin exist.

2018-02-21 | GSE107538 | GEO

Arabidopsis transcriptome changes caused by ectopic production of a turtle riboflavin-binding protein

Project description:Leaf contents of free riboflavin were modulated by ectopic expression of the turtle gene encoding riboflavin-binding protein (RfBP). Compared to Arabidopsis thaliana (L.) ecotype Col-0 (wild type), REAT (modified type) that constitutive express RfBP had 71%-77% less flavins of free form. We used microarray to investigate the influence on plants due to the reduced free flavin. One modified line (REAT11) and wild type (WT) were tested by microarray, and the experiments data revealed that abundance of transcripts for 950 genes in REAT was altered compared to the wild type.

2010-01-01 | GSE18417 | GEO

Riboflavin deficiency regulates inflammation-associated genes in rat esophageal intraepithelial neoplasia

Project description:Transcriptome analysis of RNA samples from riboflavin deficiency combined with NMBA-induced rat esophageal intraepithelial neoplasia tissues. Epidemiological studies suggest that dietary riboflavin deficiency and environmental exposure to N-nitrosomethylbenzylamine (NMBA) are common in China's high incidence area of esophageal cancer. Riboflavin deficiency has been documented as an important risk factor for esophageal cancer. In this study, we established a F344 rat esophageal tumor model that combines dietary riboflavin deficiency with exposure to NMBA. The results showed that riboflavin deficiency combined with NMBA (R0N+) enhanced the incidence of esophageal intraepithelial neoplasia, including in situ carcinoma, whereas normal levels of riboflavin combined with NMBA (RcN+) mainly induced the occurrence of esophageal benign hyperplasia and small amount of esophageal intraepithelial neoplasia. Oxidative DNA damage (8-OHdG) and DNA double-strand breaks (p-γH2AX) in R0N+ rats were higher than that in RcN+ rats. The aim of the present study is to analyze the mechanism of riboflavin deficiency-induced tumorigenesis. So, we used Affymetrix Clariom D(also known as Rat Transcriptome Array 1.0) to identify genes that were differentially expressed upon R0N+ esophageal intraepithelial neoplasia tissues.

2018-02-28 | GSE111207 | GEO

Arabidopsis transcriptome changes caused by ectopic production of a turtle riboflavin-binding protein

2010-01-01 | E-GEOD-18417 | biostudies-arrayexpress

The RNA-seq data in riboflavin-treated alcoholic liver disease

Project description:Alcoholic liver disease (ALD) is a kind serious liver disease, which will develope into the cirrhosis, liver cancer and so on. The study results show that riboflavin has the protective effect against ALD. Then the study divides the C57BL/6 mice into the three groups that were Control (C), Alcohol, Alcohol with riboflavin (AR) groups respectively. And the study makes the mouse liver RNA sequencing (RNA-seq) to find the differential expression mRNAs among three groups futher and does the related analysis in riboflavin-treated alcoholic liver disease.

2024-08-28 | GSE273208 | GEO

Hepatic Gene Expression Profiling of Riboflavin-deficient and Riboflavin-rescued Chicken Embryos at 9, 11, 13 and 15 days of incubation

Project description:This study aimed to identify key genes and pathways related to essential functions of riboflavin during the development of chicken embryos. We used as a unique model a strain of mutant chickens (rd/rd) which is unable to produce a riboflavin-binding protein and lays riboflavin-deficient eggs in which the embryos suddenly die between 13 and 15 days of incubation (e13 and e15, respectively). In these embryos, the diminished activity of flavin-dependent enzymes, particularly those associated with β-oxidation of fatty acid, limits the catabolism of yolk lipids that normally serve as the predominant source of energy required for growth. This malady leads to excessive lipid accumulation in liver and severe hypoglycemia prior to death. This lethal effect can be rescued by an injection of riboflavin just prior to incubation of fertile rd/rd eggs. Microarray-based hepatic transcriptome profiling of riboflavin-deficient (Rf-) and riboflavin-rescue (Rf+) chicken embryos were carried out at 9, 11, 13 and 15 days of incubation. Our microarray analysis identified a dramatic change in gene expression between the Rf- and Rf+ groups on e13 and e15 with 221 and 929 differentially expressed genes (DEGs), respectively. PPAR-gamma, apolipoprotein AV, adipophilin and sterol 14-alpha demethylase were up-regulated, while alpha2 antiplasmin, alpha1 antitrypsin, alpha2 microglobulin, TIP120 and GHRG1 were down-regulated in the Rf- embryos which show an increased lipid accumulation in liver that may be resulted from the disruption in fatty acid beta-oxidation. Genes involved in detoxification, the immune response and blood coagulation were down-regulated, whereas several phosphatase genes were increased. There were no apparent systematic changes in expression of genes associated with the flavin-dependent enzymes, with an exception of an increase in medium chain acyl-CoA dehydrogenase.

2017-11-05 | GSE96702 | GEO

The 16S RNA-seq data in riboflavin-treated alcoholic liver disease

Project description:Alcoholic liver disease (ALD) is a kind of liver disease that will result in liver cancer and some other high death rate liver disease. The study results show that riboflavin could protect the mouse against ALD. Then the study divides the C57BL/6 mice into the three groups including Control (C), Alcohol, Alcohol with riboflavin (AR) groups respectively. And the study makes the mouse stool samples 16S RNA sequencing (RNA-seq) to find the differential itestinal microbiota homeostasis among three groups futher and does the related analysis in riboflavin-treated alcoholic liver disease.

2024-08-28 | GSE273370 | GEO

Transcriptome profiles of a riboflavin-producing B.subtilis RH33 and wild type B.subtilis 168

Project description:The transcriptome profiles of a riboflavin-producing recombinant Bacillus subtilis RH33 and wild type Bacillus subtilis 168 were compared using DNA microarrays to identify the target genes for further enhancing riboflavin production. Transcriptome profiles of a riboflavin-producing B. subtilis RH33 were compared with those of the wild-type B. subtilis 168 as a control strain during exponentially growing period on LBG medium. These conditions corresponded to the state of high riboflavin production, which was growth related. For each comparison, two independent cultivations on LB medium with 1% glucose were performed, and exponentially growing cells (OD600 3â6) were harvested. The synthesis of cDNA and biotin-labeled cRNA were carried out exactly as described in the Affymetrix GeneChip Expression Analysis Technical Manual (2000).

2010-05-05 | E-GEOD-12873 | biostudies-arrayexpress

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