論文

国際誌
2021年5月28日

RAGE signaling antagonist suppresses mouse macrophage foam cell formation.

Biochemical and biophysical research communications
  • Nontaphat Leerach
  • Seiichi Munesue
  • Ai Harashima
  • Kumi Kimura
  • Yu Oshima
  • Shuhei Kawano
  • Mariko Tanaka
  • Akane Niimura
  • Natthiya Sakulsak
  • Hiroshi Yamamoto
  • Osamu Hori
  • Yasuhiko Yamamoto
  • 全て表示

555
開始ページ
74
終了ページ
80
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1016/j.bbrc.2021.03.139

The engagement of the receptor for advanced glycation end-products (receptor for AGEs, RAGE) with diverse ligands could elicit chronic vascular inflammation, such as atherosclerosis. Binding of cytoplasmic tail RAGE (ctRAGE) to diaphanous-related formin 1 (Diaph1) is known to yield RAGE intracellular signal transduction and subsequent cellular responses. However, the effectiveness of an inhibitor of the ctRAGE/Diaph1 interaction in attenuating the development of atherosclerosis is unclear. In this study, using macrophages from Ager+/+ and Ager-/- mice, we validated the effects of an inhibitor on AGEs-RAGE-induced foam cell formation. The inhibitor significantly suppressed AGEs-RAGE-evoked Rac1 activity, cell invasion, and uptake of oxidized low-density lipoprotein, as well as AGEs-induced NF-κB activation and upregulation of proinflammatory gene expression. Moreover, expression of Il-10, an anti-inflammatory gene, was restored by this antagonist. These findings suggest that the RAGE-Diaph1 inhibitor could be a potential therapeutic drug against RAGE-related diseases, such as chronic inflammation and atherosclerosis.

リンク情報
DOI
https://doi.org/10.1016/j.bbrc.2021.03.139
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/33813279
ID情報
  • DOI : 10.1016/j.bbrc.2021.03.139
  • PubMed ID : 33813279

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