The role of S100B in the interaction between adipocytes and macrophages

Atsushi Fujiya, Hiroshi Nagasaki, Yusuke Seino, Tetsuji Okawa, Jiro Kato, Ayako Fukami, Tatsuhito Himeno, Eita Uenishi, Shin Tsunekawa, Hideki Kamiya, Jiro Nakamura, Yutaka Oiso, Yoji Hamada

研究成果: ジャーナルへの寄稿学術論文査読

51 被引用数 (Scopus)

抄録

Objective The S100 calcium binding protein B (S100B) implicated in brain inflammation acts via the receptor of advanced glycation end products (RAGE) and is also secreted from adipocytes. We investigated the role of S100B in the interaction between adipocytes and macrophages using a cell-culture model. Design and Methods RAW264.7 macrophages (RAW) were stimulated by recombinant S100B to observe alterations in TNF-α and M1 markers; 3T3-L1 adipocytes (L1) were stimulated by TNF-α to examine S100B secretion. RAW and L1 were then mutually stimulated with conditioned media of each other, or co-cultured. The effects of S100B silencing or a RAGE-neutralizing antibody were also investigated. Results S100B upregulated TNF-α and M1 markers in RAW, and TNF-α augmented S100B secretion from L1. L1 conditioned media stimulated TNF-α secretion from RAW, and RAW conditioned media increased S100B secretion from L1. The co-culture of RAW and L1 increased TNF-α, S100B, and the expression of M1 markers and the MCP-1 receptor CCR2. The silencing of S100B or RAGE neutralization significantly ameliorated TNF-α hypersecretion from RAW that were stimulated with L1 conditioned media. Conclusions Thus, S100B as an adipokine may play a role in the interaction between adipocytes and macrophages to establish a vicious paracrine loop.

本文言語英語
ページ(範囲)371-379
ページ数9
ジャーナルObesity
22
2
DOI
出版ステータス出版済み - 02-2014

All Science Journal Classification (ASJC) codes

  • 医学(その他)
  • 内分泌学、糖尿病および代謝内科学
  • 内分泌学
  • 栄養および糖尿病

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