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Gene expression alteration in human fibroblast cells after folate depletion

ABSTRACT: The molecular basis linking folate deficiency to certain health conditions and developmental defects is complex and not fully understood. In this study, we examined the consequences of folate deficiency on global gene expression by microarray analysis and compared transcript levels in normal human fibroblast cells (GM03349) grown in folate deficient and sufficient medium. Keywords: folate depletion, stress response, comparative genomic hybridization

ORGANISM(S): Homo sapiens

PROVIDER: GSE3548 | GEO | 2006/11/02

SECONDARY ACCESSION(S): PRJNA93617

REPOSITORIES: GEO

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Folate depletion induces erythroid differentiation through perturbation of de novo purine synthesis

Project description:Folate, an essential vitamin, is a one-carbon acceptor and donor in key metabolic reactions. Erythroid cells harbor a unique sensitivity to folate deprivation, as revealed by the primary pathological manifestation of nutritional folate deprivation: megaloblastic anemia. To study this metabolic sensitivity, we applied mild folate depletion to human and mouse erythroid cell lines, and primary murine erythroid progenitors. We show that folate depletion induces early blockade of purine synthesis and accumulation of the purine synthesis intermediate and signaling molecule, AICAR, followed by enhanced heme metabolism, hemoglobin synthesis, and erythroid differentiation. This is phenocopied by inhibition of folate metabolism using the SHMT1/2 inhibitor - SHIN1, and by AICAR supplementation. Mechanistically, the metabolically-driven differentiation is independent of nucleotide sensing through mTORC1 and AMPK, and is instead mediated by protein kinase C (PKC). Our findings suggest that folate deprivation-induced premature differentiation of erythroid progenitor cells is a molecular etiology to folate-deficiency induced anemia.

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Dietary folate depletion and repletion

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Project description:We demonstrate that expression of key markers of keratinocyte differentiation is suppressed by exposure to sodium arsenite. Folate deficiency exacerbates this effect. In addition, cancer-related cell movement genes, and growth and proliferation genes are altered. Several redox-sensitive transcription factors are implicated in mediating these gene expression changes due to arsenic treatment and folate deficiency. Experiment Overall Design: K6/ODC mice were maintained on either a folate deficient or folate sufficient diet and exposed to 0, 1, or 10 ppm sodium arsenite in the drinking water for 30 days. Total RNA was isolated from skin samples and gene expression analyzed using Affymetrix Mouse 430 2.0 GeneChips. Data from 24 samples, with four mice in each of the six treatment groups, were analyzed.

2008-06-16 | E-GEOD-8733 | biostudies-arrayexpress

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Abnormal Transcriptome-wide of DNA demethylation in Folate deficiency caused neural tube defects [hMeDIP]

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Abnormal Transcriptome-wide of DNA demethylation in Folate deficiency caused neural tube defects [ChIP-seq]

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2020-01-22 | GSE125502 | GEO

Dietary folate depletion and repletion in A/J and C57BL/6J mice

Project description:Defects in homocysteine and folate metabolism are associated with increased risks for neural tube and congenital heart defects, cardiovascular disease and stroke, cancers, and neurodegeneration. In many but not all cases, dietary supplementation with folate significantly reduces the severity and incidence of these conditions. Common polymorphisms modulate these metabolic pathways and disease risks, but do not fully account for the particular birth defects and adult diseases that occur in at-risk individuals. To test whether other pathways contribute to disease pathogenesis, we analyzed global and pathway-specific changes in gene expression and levels of selected metabolites after depletion and repletion of dietary folate in two genetically distinct inbred strains of mice. Compared to the C57BL/6J strain, A/J showed greater homeostatic response to folate perturbation by retaining a higher serum folate level and minimizing global gene expression changes. Remarkably, folate perturbation led to systematic strain-specific differences only in the expression profile of the cholesterol biosynthesis pathway and translated to changes in levels of serum and liver total cholesterol. By genetically increasing serum and liver total cholesterol levels in APOE deficient mice, we modestly but significantly improved folate retention during folate depletion, suggesting an interplay between homocysteine and folate metabolism and cholesterol metabolism. Absence of measurable changes in global methylation patterns or amelioration of effects with supplementation with an alternative methyl donor suggest that dietary folate perturbations do not act through large-scale or general changes in methylation. These results suggest that homeostatic responses in cholesterol metabolism contribute to the beneficial effects of dietary folate supplementation. Keywords: time course, stress response, diet, genetic, homeostasis

2008-08-27 | GSE9242 | GEO

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