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  1. 教員研究業績
  2. 臨床薬剤学研究室
  3. 原著論文

Tumor necrosis factor-α decreases EC-SOD expression through DNA methylation.

https://gifu-pu.repo.nii.ac.jp/records/13202
https://gifu-pu.repo.nii.ac.jp/records/13202
d2e8517c-a3d3-40fc-bd14-797eb8cddb37
Item type 研究室原著論文(1)
公開日 2018-06-14
タイトル
タイトル Tumor necrosis factor-α decreases EC-SOD expression through DNA methylation.
言語
言語 eng
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_6501
資源タイプ journal article
アクセス権
アクセス権 metadata only access
アクセス権URI http://purl.org/coar/access_right/c_14cb
抄録
値 Extracellular-superoxide dismutase (EC-SOD) is a secreted antioxidative enzyme, and its presence in vascular walls may play an important role in protecting the vascular system against oxidative stress. EC-SOD expression in cultured cell lines is regulated by various cytokines including tumor necrosis factor-α (TNF-α). TNF-α is a major mediator of pathophysiological conditions and may induce or suppress the generation of various types of mediators. Epigenetics have been defined as mitotically heritable changes in gene expression that do not affect the DNA sequence, and include DNA methylation and histone modifications. The results of the present study demonstrated that TNF-α significantly decreased EC-SOD level in fibroblasts with an accompanying increase in methylated DNA. In DNA methylation and demethylation, cytosine is methylated to 5-methylcytosine (5mC) by DNA methyltransferase (DNMT), and 5mC is then converted to 5-hydroxymethylcytosine (5hmC) and cytosine in a stepwise manner by ten-eleven translocation methylcytosine dioxygenases (TETs). However, DNMT did not participate in TNF-α-induced DNA methylation within the EC-SOD promoter region. On the other hand, TNF-α significantly suppressed TET1 expression and EC-SOD mRNA levels were decreased by the silencing of TET1 in fibroblasts. These results demonstrate that the down-regulation of EC-SOD by TNF-α is regulated by DNA methylation through reductions in TET1.
書誌情報 en : Journal of clinical biochemistry and nutrition

巻 60, 号 3, p. 169-175, 発行日 2017-05
DOI
値 10.3164/jcbn.16-111
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