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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

CAPE increases the expression of SOD3 through epigenetics in human retinal endothelial cells.

https://gifu-pu.repo.nii.ac.jp/records/13181
https://gifu-pu.repo.nii.ac.jp/records/13181
e6f0cb87-014f-448f-9c33-e1d29a6c699a
Item type 研究室原著論文(1)
公開日 2018-06-14
タイトル
タイトル CAPE increases the expression of SOD3 through epigenetics in human retinal endothelial cells.
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 or SOD3), which catalyzes the dismutation of superoxide anions into hydrogen peroxide, plays a key role in vascular protection against reactive oxygen species (ROS). The excess generation of ROS is closely involved in the pathogenesis of diabetic retinopathy (DR); therefore, the maintenance of SOD3 expression at high levels is important for the prevention of DR. In the present study, we showed that caffeic acid phenethyl ester (CAPE) increased the expression of SOD3 through the acetylation of histone within the SOD3 promoter region in human retinal endothelial cells (HRECs). Histone acetylation within its promoter was focused on the inhibition of histone deacetylase (HDAC), and we examined the involvement of myocyte enhancer factor 2 (MEF2) and HDAC1 in CAPE-elicited SOD3 expression. Our results demonstrate that SOD3 silencing in basal HRECs is regulated by HDAC1 composed with MEF2A/2D hetero dimers. Moreover, phosphorylation of threonine 312 in MEF2A and dissociation of HDAC1 from SOD3 promoter play pivotal roles in CAPE-elicited SOD3 expression. Overall, our findings provide that CAPE may be one of the seed compounds that maintain redox homeostasis.
書誌情報 en : Journal of clinical biochemistry and nutrition

巻 61, 号 1, p. 6-13, 発行日 2017-07
DOI
値 10.3164/jcbn.16-109
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