論文

査読有り
2017年7月

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

JOURNAL OF CLINICAL BIOCHEMISTRY AND NUTRITION
  • Atsuko Ohashi
  • ,
  • Hiroyuki Yasuda
  • ,
  • Tetsuro Kamiya
  • ,
  • Hirokazu Hara
  • ,
  • Tetsuo Adachi

61
1
開始ページ
6
終了ページ
13
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.3164/jcbn.16-109
出版者・発行元
JOURNAL CLINICAL BIOCHEMISTRY & NUTRITION

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.

Web of Science ® 被引用回数 : 2

リンク情報
DOI
https://doi.org/10.3164/jcbn.16-109
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/28751803
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000405648000002&DestApp=WOS_CPL