Article
Regional expression of brain derived neurotrophic factor (BDNF) is correlated with dynamic patterns of promoter methylation in the developing mouse forebrain.
Vanderbilt Kennedy Center for Research on Human Development and Department of Pharmacology, Vanderbilt University School of Medicine, 465 21st Avenue S. MRBIII, Rm 8114, Nashville, TN 37232, USA.
Molecular Brain Research (impact factor:
2).
11/2005;
140(1-2):1-9.
DOI:10.1016/j.molbrainres.2005.06.014
pp.1-9
Source: PubMed
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Citations (0)
- Cited In (3)
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Article: Epigenetic alterations of the dopaminergic system in major psychiatric disorders.
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ABSTRACT: Although there is evidence to link schizophrenia (SCZ) and bipolar disorder (BD) to genetic and environmental factors, specific individual or groups of genes/factors causative of the disease have been elusive to the research community. An understanding of the molecular aberrations that cause these mental illnesses requires comprehensive approaches that examine both genetic and epigenetic factors. Because of the overwhelming evidence for the role of environmental factors in the disease presentation, our initial approach involved deciphering how epigenetic changes resulting from promoter DNA methylation affect gene expression in SCZ and BD. Apparently, the central reversible but covalent epigenetic modification to DNA is derived from methylation of the cytosine residues that is potentially heritable and can affect gene expression and downstream activities. Environmental factors can influence DNA methylation patterns and hence alter gene expression. Such changes can be especially problematic in individuals with genetic susceptibilities to specific diseases. Recent reports from our laboratory provided compelling evidence that both hyper- and hypo-DNA methylation changes of the regulatory regions play critical roles in defining the altered functionality of genes in major psychiatric disorders such as SCZ and BD. In this chapter, we outline the technical details of the methods that could help to expand this line of research to assist with compiling the differential methylation-mediated epigenetic alterations that are responsible for the pathogenesis of SCZ, BD, and other mental diseases. We use the genes of the extended dopaminergic (DAergic) system such as membrane-bound catechol-O-methyltransferase (MB-COMT), monoamine oxidase A (MAOA), dopamine transporter 1 (DAT1), tyrosine hydroxylase (TH), dopamine (DA) receptors1 and 2 (DRD1/2), and related genes (e.g., reelin [RELN] and brain-derived neurotrophic factor [BDNF]) to illustrate the associations between differential promoter DNA methylations and disease phenotype. It is our hope that comprehensive analyses of the DAergic system as the prototype could provide the impetus and molecular basis to uncover early markers for diagnosis, help in the understanding of differences in disease severity in individuals with similar or identical genetic makeup, and assist with the identification of novel targets for therapeutic applications.Methods in molecular biology (Clifton, N.J.) 02/2008; 448:187-212. -
Article: Lasting epigenetic influence of early-life adversity on the BDNF gene.
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ABSTRACT: Childhood maltreatment and early trauma leave lasting imprints on neural mechanisms of cognition and emotion. With a rat model of infant maltreatment by a caregiver, we investigated whether early-life adversity leaves lasting epigenetic marks at the brain-derived neurotrophic factor (BDNF) gene in the central nervous system. During the first postnatal week, we exposed infant rats to stressed caretakers that predominately displayed abusive behaviors. We then assessed DNA methylation patterns and gene expression throughout the life span as well as DNA methylation patterns in the next generation of infants. Early maltreatment produced persisting changes in methylation of BDNF DNA that caused altered BDNF gene expression in the adult prefrontal cortex. Furthermore, we observed altered BDNF DNA methylation in offspring of females that had previously experienced the maltreatment regimen. These results highlight an epigenetic molecular mechanism potentially underlying lifelong and transgenerational perpetuation of changes in gene expression and behavior incited by early abuse and neglect.Biological psychiatry 02/2009; 65(9):760-9. · 8.93 Impact Factor -
Article: Biological functions and transcriptional targets of CaRF in neurons.
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ABSTRACT: Calcium-response factor (CaRF) is a unique DNA-binding protein first recognized as a transcription factor for its role in modulating transcription of the gene encoding Brain-Derived Neurotrophic Factor (BDNF) in neurons. Here I review evidence for the biological functions and transcriptional targets of CaRF in the brain and discuss potential mechanisms by which calcium-activated signaling pathways may modulate CaRF-dependent transcription. These data paint an emerging picture of CaRF as a regulatory nexus for signaling pathways that control aspects of synaptic development and neuronal function.Cell calcium 05/2011; 49(5):290-5. · 4.29 Impact Factor
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Keywords
BDNF complex promoter
BDNF expression
BDNF gene expression
BDNF promoter
Brain Derived Neurotrophic Factor
brain development
CpG dinucleotides
developing mouse forebrain
differential expression
differential methylation
DNA methylation
epigenetic control mechanism
forebrain development
gene promoters
methylation
mouse BDNF promoter
mouse forebrain
normal differential expression
regulatory controls
regulatory region
