1,721,023 research outputs found
Epigenetics and nutrition: B-vitamin deprivation and its impact on brain amyloid
No full textEpigenetics is becoming the epicentre of modern medicine because it is beginning to clarify the relationship between genetic background, environment, aging, and disease. SAM-dependent DNA methylation at the 5-position of cytosine within CpG dinucleotides represents an important mechanism for epigenetic control of gene expression and maintenance of genome integrity. Hence, methyl deficiency leads to disturbances in gene expression. B vitamins (B12, B6, and folate) have a pivotal role in reducing homocysteine accumulation by remethylation to form methionine and by transsulfuration to form glutathione (GSH). B vitamins have therefore a central function in SAM synthesis, in gene expression, and in the synthesis of one of the major antioxidant molecules. The physiological causes of AD onset are not yet well understood, but it has been shown that changes in DNA methylation due to vitamin deficiency contributes to the basic mechanisms responsible for AD onset. Accordingly, restoration of gene methylation pattern could be a target for preventing AD or arresting the progression of disease. A methyl donor such as SAM can repair the DNA methylation pattern and thereby restore normal biological functions in AD mice. Recent studies indicate that B vitamin deprivation and SAM supplementation, which modify the SAM cycle, can influence amyloidogenesis in mice, probably via SAM-dependent methylation reactions. SAM supplementation has been shown to reduce beta amyloid in mice brain
S-adenosylmethionine and derivatives thereof for the treatment and prevention of Alzheimer Disease
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The differentiation of LS/A10 myoblast cell line (a subclone of L5 line) is controlled by changes of cultural conditions
No full textWe report here that it is possible to induce differentiation in a subline of L5 myoblast line (L5/A10) by manipulating the culture media. When L5/A10 myoblasts are cultured in F14 supplemented with 10% fetal calf serum the cells grow with a division time of 12 h and reach confluency at a cell density of approximately 2.4 x 105 cells per cm2, without undergoing differentiation, characterized, morphologically, by formation of multinucleated fibers, and biochemically, by the synthesis of muscle specific proteins such as creatinine phosphokinase or myokinase. However, cells, grown in F14 + 10% fetal calf serum, will undergo regular differentiation after a limited number of division when transferred to F14 medium supplemented with limiting concentrations (1-2%) of fetal calf serum. Investigations of the biochemistry of myoblast differentiation in cell culture will be facilitated by the availability of a cell line that can undergo differentiation under controlled conditions
One-carbon metabolism and Alzheimer's disease: is it all a methylation matter?
No full textThe sporadic form of Alzheimer disease, late onset Alzheimer's disease (LOAD), is a multifactorial disease; a strong link between nutritional and genetic factors with normal aging and dementia is supported by studies on nutrition, metabolism, and neurodegeneration. Specifically, the involvement of homocysteine (HCY) and its dietary determinants (vitamins B6, B12, and folate, besides methionine) in dementia has been a topic of intense investigation. In this Commentary we would like to highlight the role of 1-carbon metabolism in epigenetics and Alzheimer's disease and evidence the coinvolvement of this metabolism in amyloid and tau pathways. (C) 2011 Elsevier Inc. All rights reserved
Erythroid differentiation and regulatory gene expression are modulated by adenosine derivatives interfering with S-adenosylmethionine metabolic pathway
No full textThe differentiation of murine erythroleukemia cells and the expression of SCL, Id1 and c-myc regulatory genes were studied. The first gene is a positive regulator of differentiation, while the other two are both negative regulators of differentiation and positive regulators of proliferation. Accordingly, our data show that when differentiation is stimulated SCL is upregulated while Id1 and c-myc are, coordinately, downregulated. The cultures were treated with two adenosine derivatives, 3-deazaadenosine and 3-deazaaristeromycin, known to act on the metabolic pathway of the methyl donor S-adenosylmethionin, in order to assess the possibility of a coordinated modulation, by these drugs, of regulatory gene expression and erythroid cell differentiation. 3-Deazaaristeromycin caused the simultaneous downregulation of Id1 and c-myc, whereas 3-deazaadenosine caused their upregulation; both drugs produced a transient increase in SCL expression. The use of these drugs evidenced a predominant regulatory effect of negative regulators in the control of erythroid differentiation. The distinct effects of the two drugs on regulatory gene expression led to an increased differentiation induced by 3-deazaaristeromycin and to a reduced differentiation induced by 3-deazaadenosine, if compared with controls. Southern analysis of DNA digested with methylation-specific restriction endonucleases showed that the administration of 3-deazaaristeromycin resulted in hypomethylation of SCL and c-myc, thus evidencing, in these cells, a clear correlation between DNA hypomethylation and differentiation but no straightforward correlation between DNA methylation and gene expression
Analysis by two dimensional gel electrophoresis of developmentally regulated membrane proteins in L5/3C4 myoblast cell line
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