Dietary vitamin A impacts DNA methylation patterns of adipogenesis-related genes in suckling rats

Arreguín, Andrea; Ribot, Joan; Mušinović, Hana; Lintig, Johannes von; Palou, Andreu; Bonet, M. Luisa

doi:10.1016/j.abb.2018.05.009

Cited by 20 publications

(11 citation statements)

References 49 publications

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“…Vitamin A Influence on global and site-specific DNA methylation profiles. [763,764] Retinoic acid Regulation of epigenetic processes, including DNA methylation, histone modifications, the formation of polycomb repressive complex 2, and induction of transcription factors.…”

Section: Vitamins and Their Derivativesmentioning

confidence: 99%

Genome-Protecting Compounds as Potential Geroprotectors

Proshkina

Shaposhnikov

Moskalev

2020

IJMS

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Throughout life, organisms are exposed to various exogenous and endogenous factors that cause DNA damages and somatic mutations provoking genomic instability. At a young age, compensatory mechanisms of genome protection are activated to prevent phenotypic and functional changes. However, the increasing stress and age-related deterioration in the functioning of these mechanisms result in damage accumulation, overcoming the functional threshold. This leads to aging and the development of age-related diseases. There are several ways to counteract these changes: (1) prevention of DNA damage through stimulation of antioxidant and detoxification systems, as well as transition metal chelation; (2) regulation of DNA methylation, chromatin structure, non-coding RNA activity and prevention of nuclear architecture alterations; (3) improving DNA damage response and repair; (4) selective removal of damaged non-functional and senescent cells. In the article, we have reviewed data about the effects of various trace elements, vitamins, polyphenols, terpenes, and other phytochemicals, as well as a number of synthetic pharmacological substances in these ways. Most of the compounds demonstrate the geroprotective potential and increase the lifespan in model organisms. However, their genome-protecting effects are non-selective and often are conditioned by hormesis. Consequently, the development of selective drugs targeting genome protection is an advanced direction.

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Section: Vitamins and Their Derivativesmentioning

confidence: 99%

Genome-Protecting Compounds as Potential Geroprotectors

Proshkina

Shaposhnikov

Moskalev

2020

IJMS

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“…Conversely, in β-carotene-treated rats hypomethylation of RBP4 and hypermethylation of PCNA promoters at distinct CpGs were found, while the expression of PPARG2 was not affected. Finally, in both treated groups, ZFP423 promoter was found to be hypomethylated, with a consequently increased gene expression [40].…”

Section: Epigenetics and Adipogenesismentioning

confidence: 89%

“…It has been demonstrated that among the micronutrients vitamin A, and in particular its bioactive form retinoic acid (RA), modulates the methylation of genes involved in development and metabolism [40]. Arreguin et al demonstrated that rats, supplemented with retinyl ester or β-carotene during the suckling period, showed inWAT altered methylation profiles of CpG islands of PPARG (a gene involved in adipogenic differentiation), ZFP423 (a gene involved in adipogenic determination), PCNA (a gene involved in proliferation), and RBP4 (a gene involved in retinol transport).…”

Section: Epigenetics and Adipogenesismentioning

confidence: 99%

Molecular and Lifestyle Factors Modulating Obesity Disease

et al. 2020

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Obesity adversely affects bone health by means of multiple mechanisms, e.g., alterations in bone-regulating hormones, inflammation, and oxidative stress. Substantial evidence supports the relationship between adiposity and bone disorders in overweight/obese individuals. It is well known that the balance between mutually exclusive differentiation of progenitor cells into osteoblasts or adipocytes is controlled by different agents, including growth factors, hormones, genetic and epigenetic factors. Furthermore, an association between vitamin D deficiency and obesity has been reported. On the other hand, regular physical activity plays a key role in weight control, in the reduction of obesity-associated risks and promotes osteogenesis. The aim of this review is to highlight relevant cellular and molecular aspects for over-weight containment. In this context, the modulation of progenitor cells during differentiation as well as the role of epigenetics and microbiota in obesity disease will be discussed. Furthermore, lifestyle changes including an optimized diet as well as targeted physical activity will be suggested as strategies for the treatment of obesity disease.

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“…In addition, ATRA is a metabolite of vitamin A and functions to support normal pattern formation during embryogenesis, cellular differentiation and proliferation 36 . ATRA affects global and gene-specific DNA methylation and increased expression of suppressor of variegation 3-9 homolog 2 (SUV39H2) that induces the inhibitory mark trimethylation of histone 3 lysine 9 (H3K9me3) 37 , 38 . Several studies have confirmed that ATRA induces cell cycle arrest in embryonic palatal mesenchymal (MEPM) to cause development of cleft palate 39 .…”

Section: Discussionmentioning

confidence: 99%

DNA hypermethylation of Fgf16 and Tbx22 associated with cleft palate during palatal fusion

et al. 2019

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Objective:Cleft palate (CP) is a congenital birth defect caused by the failure of palatal fusion. Little is known about the potential role of DNA methylation in the pathogenesis of CP. This study aimed to explore the potential role of DNA methylation in the mechanism of CP.Methodology:We established an all-trans retinoic acid (ATRA)-induced CP model in C57BL/6J mice and used methylation-dependent restriction enzymes (MethylRAD, FspEI) combined with high-throughput sequencing (HiSeq X Ten) to compare genome-wide DNA methylation profiles of embryonic mouse palatal tissues, between embryos from ATRA-treated vs. untreated mice, at embryonic gestation day 14.5 (E14.5) (n=3 per group). To confirm differentially methylated levels of susceptible genes, real-time quantitative PCR (qPCR) was used to correlate expression of differentially methylated genes related to CP.Results:We identified 196 differentially methylated genes, including 17,298 differentially methylated CCGG sites between ATRA-treated vs. untreated embryonic mouse palatal tissues (P<0.05, log2FC>1). The CP-related genes Fgf16 (P=0.008, log2FC=1.13) and Tbx22 (P=0.011, log2FC=1.64,) were hypermethylated. Analysis of Fgf16 and Tbx22, using Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG), identified 3 GO terms and 1 KEGG pathway functionally related to palatal fusion. The qPCR showed that changes in expression level negatively correlated with methylation levels.Conclusions:Taken together, these results suggest that hypermethylation of Fgf16 and Tbx22 is associated with decreased gene expression, which might be responsible for developmental failure of palatal fusion, eventually resulting in the formation of CP.

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Dietary vitamin A impacts DNA methylation patterns of adipogenesis-related genes in suckling rats

Cited by 20 publications

References 49 publications

Genome-Protecting Compounds as Potential Geroprotectors

Genome-Protecting Compounds as Potential Geroprotectors

Molecular and Lifestyle Factors Modulating Obesity Disease

DNA hypermethylation of Fgf16 and Tbx22 associated with cleft palate during palatal fusion

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