論文

査読有り
2016年11月

Suppression of EC-SOD by oxLDL During Vascular Smooth Muscle Cell Proliferation

JOURNAL OF CELLULAR BIOCHEMISTRY
  • Junya Makino
  • ,
  • Rei Asai
  • ,
  • Mao Hashimoto
  • ,
  • Tetsuro Kamiya
  • ,
  • Hirokazu Hara
  • ,
  • Masayuki Ninomiya
  • ,
  • Mamoru Koketsu
  • ,
  • Tetsuo Adachi

117
11
開始ページ
2496
終了ページ
2505
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1002/jcb.25542
出版者・発行元
WILEY-BLACKWELL

Reactive oxygen species (ROS) produced by endothelial cells and macrophages play important roles in atherogenesis because they promote the formation of oxidized low-density lipoproteins (oxLDL). Extracellular-superoxide dismutase (EC-SOD) is mainly produced by vascular smooth muscle cells (VSMCs), is secreted into the extracellular space, and protects cells from the damaging effects of the superoxide anion. Thus, the expression of EC-SOD in VSMCs is crucial for protecting cells against atherogenesis; however, oxLDL-induced changes in the expression of EC-SOD in VSMCs have not yet been examined. We herein showed that oxLDL decreased EC-SOD mRNA and protein levels by binding to lectin-like oxidized LDL receptor-1 (LOX-1). Moreover, we demonstrated the significant role of mitogen-activated protein kinase (MEK)/extracellular-regulated protein kinase (ERK) signaling in oxLDL-elicited reductions in the expression of EC-SOD and proliferation of VSMCs. The results obtained with the FCS treatment indicate that oxLDL-elicited reductions in the expression of EC-SOD are related to the proliferation of VSMCs. We herein showed for the first time that luteolin, a natural product, restored oxLDL-induced decreases in the expression of EC-SOD and proliferation of VSMCs. Collectively, the results of the present study suggest that oxLDL accelerates the development of atherosclerosis by suppressing the expression of EC-SOD and also that luteolin has potential as a treatment for atherosclerosis. J. Cell. Biochem. 117: 2496-2505, 2016. (c) 2016 Wiley Periodicals, Inc.

Web of Science ® 被引用回数 : 12

リンク情報
DOI
https://doi.org/10.1002/jcb.25542
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/26990420
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000383626800006&DestApp=WOS_CPL