The role of S100B in the interaction between adipocytes and macrophages

Abstract

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-a and M1 markers; 3T3-L1 adipocytes (L1) were stimulated by TNF-a 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-a and M1 markers in RAW, and TNF-a augmented S100B secretion from L1. L1 conditioned media stimulated TNF-a secretion from RAW, and RAW conditioned media increased S100B secretion from L1. The co-culture of RAW and L1 increased TNF-a, S100B, and the expression of M1 markers and the MCP-1 receptor CCR2. The silencing of S100B or RAGE neutralization significantly ameliorated TNF-a 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.

Putative model for heat shock protein 70 complexation with receptor of advanced glycation end products through fluorescence proximity assays and normal mode analyses

“…Our previous studies (Grunwald et al 2014) showed that macrophages treated with preoxidized HSP70 exhibited a different pattern of activation compared with that of macrophages treated with HSP70, with lower cell proliferation and viability, lower levels of TNF-α release, and lower phagocytic activity. Similar results, including increased secretion of TNF-α and increased phagocytosis, have been observed in macrophages upon RAGE ligand binding (Fujiya et al 2014;Ma et al 2012;Tang et al 2010), suggesting that RAGE may have unidentified interactions associated with specific signaling pathways.…”

First Evidence For Glial Pathology In Late Life Minor Depression: s100b Is Increased In Males With Minor Depression

“…S100B is secreted by adipocytes and is involved in the pathogenesis of obesity as shown in vitro (Fujiya et al, 2014) and in vivo (Buckman et al, 2014). Positive correlation of serum S100B with BMI was previously reported in a combined sample of cognitively intact lean and obese subjects (Steiner et al, 2010a) and in subjects with schizophrenia (Steiner et al, 2010b).…”

“…For instance, various subtypes of leukocytes can secrete S100B (Miki et al, 2013;Fujiya et al, 2014;Moutsatsou et al, 2014). Thrombocytes are the largest source for serum BDNF (Fujimura et al, 2002), adipocytes produce both S100B and BDNF (Fujiya et al, 2014;Huang et al, 2014), finally NSE may originate from damaged peripheral nerves (Li et al, 2013). Because we did not assume relevant biases related to these potentially confounding sources in minor depression, we did not control for potential non-brain sources of the serum markers in our study.…”

Age-related accumulation of advanced glycation end-products-albumin, S100β, and the expressions of advanced glycation end product receptor differ in visceral and subcutaneous fat

“…In addition, the RAGE pathway is involved in mouse adipocyte hypertrophy and insulin sensitivity [6], but few studies compare the AGE-albumin accumulations, level of S100b, and RAGE expressions of different adipocyte types. Therefore we focused on how age-related AGE-albumin accumulation level of S100b, and RAGE expression differ in visceral and subcutaneous fat.…”

“…One recent study suggests that adipocyte derived S100b can act as an inflammatory cytokine via RAGE and stimulate M1 polarization of macrophages which is a classical feature of activation in an in vitro co-culture system [5,6].…”