Eating greens alters genes

Jabr, Ferris

doi:10.1016/s0262-4079(11)62373-7

Cited by 1 publication

(4 citation statements)

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“…Short interfering RNAs, are a class of double-strnded RNA (dsRNA) molecules, that can guide methylation to complementary DNA, were first elucidated in plants, to enable the precise targeting of gene action [ 164 ]. Plant - derived miRNAs which enter the blood stream have been shown to muffle or amplify gene expression by binding to strands of messenger RNA with potential for therapy [ 53 ].…”

Section: Appendix Vmentioning

confidence: 99%

“…Epigenetics is now generally defined as information heritable during cell division but not contained within the DNA sequence itself [ 14 ]. There are three major ways organisms alter their DNAs inherited messages: enzymes methylate DNA to modulate transcription; histone modifications and nucleosome positioning to induce or repress target sequences; and non-coding small RNAs (including microRNAs and short interfering RNAs) which attach themselves to messenger RNA to modify the expression of specific genes [ 10 , 46 , 52 , 53 ]. DNA-cytosine methylation is a central epigenetic modification that has essential roles in cellular processes including genome regulation, development and disease [ 54 ].…”

Section: Introductionmentioning

confidence: 99%

“…Good dietary practices and optimal nutritional status are known to promote growth and tissue development, as well as disease prevention [ 39 , 53 , 103 , 104 ]. Nutritional epigenetics has emerged as a novel mechanism underlying gene-diet interactions [ 104 ] with the strongest evidence for transgenerational inheritance coming from the survivors of the Dutch Hunger Winter [ 105 ].…”

Section: Introductionmentioning

confidence: 99%

“…Nutritional epigenetics has emerged as a novel mechanism underlying gene-diet interactions [ 104 ] with the strongest evidence for transgenerational inheritance coming from the survivors of the Dutch Hunger Winter [ 105 ]. Dietary modification can have a profound effect on DNAm and genomic imprinting [ 16 , 106 ], with plant-derived microRNAs entering the bloodstream [ 53 ]. A major focus of research on dietary influences on epigenetic status has been on nutrition in utero , because the epigenome is probably malleable particularly during this life-course window [ 60 , 107 , 108 ], and because epigenetic marking by early exposures is a compelling mechanism underlying effects on lifelong health [ 108 , 109 ].…”

Section: Introductionmentioning

confidence: 99%

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Adolescent idiopathic scoliosis (AIS), environment, exposome and epigenetics: a molecular perspective of postnatal normal spinal growth and the etiopathogenesis of AIS with consideration of a network approach and possible implications for medical therapy

et al. 2011

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Genetic factors are believed to play an important role in the etiology of adolescent idiopathic scoliosis (AIS). Discordant findings for monozygotic (MZ) twins with AIS show that environmental factors including different intrauterine environments are important in etiology, but what these environmental factors may be is unknown. Recent evidence for common chronic non-communicable diseases suggests epigenetic differences may underlie MZ twin discordance, and be the link between environmental factors and phenotypic differences. DNA methylation is one important epigenetic mechanism operating at the interface between genome and environment to regulate phenotypic plasticity with a complex regulation across the genome during the first decade of life. The word exposome refers to the totality of environmental exposures from conception onwards, comprising factors in external and internal environments. The word exposome is used here also in relation to physiologic and etiopathogenetic factors that affect normal spinal growth and may induce the deformity of AIS. In normal postnatal spinal growth we propose a new term and concept, physiologic growth-plate exposome for the normal processes particularly of the internal environments that may have epigenetic effects on growth plates of vertebrae. In AIS, we propose a new term and concept pathophysiologic scoliogenic exposome for the abnormal processes in molecular pathways particularly of the internal environment currently expressed as etiopathogenetic hypotheses; these are suggested to have deforming effects on the growth plates of vertebrae at cell, tissue, structure and/or organ levels that are considered to be epigenetic. New research is required for chromatin modifications including DNA methylation in AIS subjects and vertebral growth plates excised at surgery. In addition, consideration is needed for a possible network approach to etiopathogenesis by constructing AIS diseasomes. These approaches may lead through screening, genetic, epigenetic, biochemical, metabolic phenotypes and pharmacogenomic research to identify susceptible individuals at risk and modulate abnormal molecular pathways of AIS. The potential of epigenetic-based medical therapy for AIS cannot be assessed at present, and must await new research derived from the evaluation of epigenetic concepts of spinal growth in health and deformity. The tenets outlined here for AIS are applicable to other musculoskeletal growth disorders including infantile and juvenile idiopathic scoliosis.

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Section: Appendix Vmentioning

confidence: 99%