CNP and DPYSL2 mRNA Expression and Promoter Methylation Levels in Brain of Alzheimer's Disease Patients

Silva, Patrícia Natália; Furuya, Tatiane Katsue; Braga, Ianna Sampaio; Rasmussen, Lucas Trevizani; Lábio, Roger Willian de; Bertolucci, Paulo Henrique Ferreira; Chen, Elizabeth; Turecki, Gustavo; Mechawar, Naguib; Payão, Spencer Luíz Marques; Mill, Jonathan; Smith, Marı́lia de Arruda Cardoso

doi:10.3233/jad-2012-121192

Cited by 28 publications

(10 citation statements)

References 15 publications

(2 reference statements)

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“…These genes include synaptosomal-associated protein 25 ( SNAP-25 ) (Furuya et al, 2012b), SIRT3 , SMARCA5 , CDH1 (Silva et al, 2008), 2′,3′-cyclic-nucleotide 3′-phosphodiesterase ( CNP ), and dihydropyrimidinase-like 2 ( DPYSL2 ) (Silva et al, 2013). …”

Section: Dna Methylation and Alzheimer's Diseasementioning

confidence: 99%

DNA methylation, a hand behind neurodegenerative diseases

Lu¹,

Liu²,

Y³

et al. 2013

Front. Aging Neurosci.

139

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Epigenetic alterations represent a sort of functional modifications related to the genome that are not responsible for changes in the nucleotide sequence. DNA methylation is one of such epigenetic modifications that have been studied intensively for the past several decades. The transfer of a methyl group to the 5 position of a cytosine is the key feature of DNA methylation. A simple change as such can be caused by a variety of factors, which can be the cause of many serious diseases including several neurodegenerative diseases. In this review, we have reviewed and summarized recent progress regarding DNA methylation in four major neurodegenerative diseases: Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), and amyotrophic lateral sclerosis (ALS). The studies of these four major neurodegenerative diseases conclude the strong suggestion of the important role DNA methylation plays in these diseases. However, each of these diseases has not yet been understood completely as details in some areas remain unclear, and will be investigated in future studies. We hope this review can provide new insights into the understanding of neurodegenerative diseases from the epigenetic perspective.

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Section: Dna Methylation and Alzheimer's Diseasementioning

confidence: 99%

DNA methylation, a hand behind neurodegenerative diseases

Lu¹,

Liu²,

Y³

et al. 2013

Front. Aging Neurosci.

139

View full text Add to dashboard Cite

show abstract

“…In turn, CAPS-1 is a calcium-binding protein engaged in exocytosis of neurotransmitters and neuropeptides, while CNP is required for proper axoglial interactions [45]. Decreased CNP expression, observed in entorhinal and auditory cortex of AD patients, might suggest the impairment in myelination with subsequent synaptic and cognition loss [46]. It is worth highlighting that in our study CNP was a common protein differentially expressed in the Hp of control mice, apoE −/− mice, and apoE −/− mice treated with Alda-1.…”

Section: Discussionmentioning

confidence: 99%

Proteomic Analysis of Mitochondria-Enriched Fraction Isolated from the Frontal Cortex and Hippocampus of Apolipoprotein E Knockout Mice Treated with Alda-1, an Activator of Mitochondrial Aldehyde Dehydrogenase (ALDH2)

Stachowicz

Olszanecki

Suski

et al. 2017

IJMS

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The role of different genotypes of apolipoprotein E (apoE) in the etiology of Alzheimer’s disease is widely recognized. It has been shown that altered functioning of apoE may promote 4-hydroxynonenal modification of mitochondrial proteins, which may result in mitochondrial dysfunction, aggravation of oxidative stress, and neurodegeneration. Mitochondrial aldehyde dehydrogenase (ALDH2) is an enzyme considered to perform protective function in mitochondria by the detoxification of the end products of lipid peroxidation, such as 4-hydroxynonenal and other reactive aldehydes. The goal of our study was to apply a differential proteomics approach in concert with molecular and morphological techniques to elucidate the changes in the frontal cortex and hippocampus of apolipoprotein E knockout (apoE−/−) mice upon treatment with Alda-1—a small molecular weight activator of ALDH2. Despite the lack of significant morphological changes in the brain of apoE−/− mice as compared to age-matched wild type animals, the proteomic and molecular approach revealed many changes in the expression of genes and proteins, indicating the impairment of energy metabolism, neuroplasticity, and neurogenesis in brains of apoE−/− mice. Importantly, prolonged treatment of apoE−/− mice with Alda-1 led to the beneficial changes in the expression of genes and proteins related to neuroplasticity and mitochondrial function. The pattern of alterations implies mitoprotective action of Alda-1, however, the accurate functional consequences of the revealed changes require further research.

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“…Pearson correlation and t Student test were carried out using (SPSS) software (IBM SPSS 22, SPSS Inc., Chicago, IL., USA) and values of P < 0.05 were considered statistically significant. 28 …”

Section: Methodsmentioning

confidence: 99%

Relationship of hypomethylation CpG islands in interleukin-6 gene promoter withIL-6mRNA levels in patients with coronary atherosclerosis

Mohammadpanah

Heidari

Khatami

et al. 2020

J Cardiovasc Thorac Res

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Introduction: Atherosclerosis is the important cause of most cardiovascular diseases, with high prevalence and mortality. Atherosclerosis is not only a lipid metabolism disorder but also recently is defined as a chronic inflammatory disease. Several studies showed that interleukin-6 (IL-6) is involved in the pathogenesis of atherosclerosis. The aim of the present study is the examination of IL6 mRNA Levels and hypomethylation of IL6 promoter in atherosclerosis patients. Methods: In this assay, a total of 35 cases with atherosclerosis and 30 controls were enrolled. RNA and DNA were isolated from the peripheral blood of all samples. Mean IL6 gene expression was determined by RT-PCR and methylation status at six CpG motifs in IL6 promoter was determined using bisulfite genomic sequencing. Results: Real Time-PCR analysis results showed the mean IL6 RNA level in atherosclerosis patients candidate for CABG (coronary artery bypass grafting) was significantly higher than controls ( P value = 0.01). Also, the upstream CpG motifs (-1038 to -952) in IL6 promoter were predominantly unmethylated in patients than in the controls ( P value = 0.01). Conclusion: These findings suggest that an increase in IL-6 gene expression and its DNA hypomethylation promoter are associated with atherosclerosis patient’s candidate for CABG surgery.

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CNP and DPYSL2 mRNA Expression and Promoter Methylation Levels in Brain of Alzheimer's Disease Patients

Cited by 28 publications

References 15 publications

DNA methylation, a hand behind neurodegenerative diseases

DNA methylation, a hand behind neurodegenerative diseases

Proteomic Analysis of Mitochondria-Enriched Fraction Isolated from the Frontal Cortex and Hippocampus of Apolipoprotein E Knockout Mice Treated with Alda-1, an Activator of Mitochondrial Aldehyde Dehydrogenase (ALDH2)

Relationship of hypomethylation CpG islands in interleukin-6 gene promoter withIL-6mRNA levels in patients with coronary atherosclerosis

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