論文

査読有り
2016年11月

Exendin-4 induces extracellular-superoxide dismutase through histone H3 acetylation in human retinal endothelial cells

JOURNAL OF CLINICAL BIOCHEMISTRY AND NUTRITION
  • Hiroyuki Yasuda
  • ,
  • Atsuko Ohashi
  • ,
  • Shohei Nishida
  • ,
  • Tetsuro Kamiya
  • ,
  • Tetsuya Suwa
  • ,
  • Hirokazu Hara
  • ,
  • Jun Takeda
  • ,
  • Yoshinori Itoh
  • ,
  • Tetsuo Adachi

59
3
開始ページ
174
終了ページ
181
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.3164/jcbn.16-26
出版者・発行元
JOURNAL CLINICAL BIOCHEMISTRY & NUTRITION

Extracellular-superoxide dismutase (genetic name SOD3) is a secreted anti-oxidative enzyme, and its presence in vascular walls may play an important role in protecting the vascular system against oxidative stress. Oxidative stress has been implicated in the pathogenesis of diabetic retinopathy; therefore, increases in extracellular-superoxide dismutase have been suggested to inhibit the progression of diabetic retinopathy. Incretin-based drugs such as glucagon-like peptide-1 receptor agonists are used in the treatment of type 2 diabetes. Glucagon-like peptide-1 receptor agonists are expected to function as extrapancreatic agents because the glucagon-like peptide-1 receptor is expressed not only in pancreatic tissues, but also in many other tissue types. We herein demonstrated that exendin-4, a glucagon-like peptide-1 receptor agonist, induced the expression of extracellular-superoxide dismutase in human retinal microvascular endothelial cells through epigenetic regulation. The results of the present study demonstrated that exendin-4 induced the expression of extracellularsuperoxide dismutase through histone H3 acetylation at the SOD3 proximal promoter region. Moreover, plasma extracellularsuperoxide dismutase concentrations in diabetic patients were elevated by incretin-based therapies. Therefore, incretin-based therapies may exert direct extrapancreatic effects in order to protect blood vessels by enhancing anti-oxidative activity.

Web of Science ® 被引用回数 : 13

リンク情報
DOI
https://doi.org/10.3164/jcbn.16-26
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/27895384
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000390084300004&DestApp=WOS_CPL