Open Access

Nicotinic α7 receptor inhibits the acylation stimulating protein‑induced production of monocyte chemoattractant protein‑1 and keratinocyte‑derived chemokine in adipocytes by modulating the p38 kinase and nuclear factor‑κB signaling pathways

  • Authors:
    • Zhou‑Yang Jiao
    • Jing Wu
    • Chao Liu
    • Bing Wen
    • Wen‑Zeng Zhao
    • Xin‑Ling Du
  • View Affiliations

  • Published online on: August 12, 2016     https://doi.org/10.3892/mmr.2016.5630
  • Pages: 2959-2966
  • Copyright: © Jiao et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Obesity is associated with chronic low‑grade inflammation, which is characterized by increased infiltration of macrophages into adipose tissue. Acylation stimulating protein (ASP) is an adipokine derived from the immune complement system, which constitutes a link between adipocytes and macrophages, and is involved in energy homeostasis and inflammation. The purpose of the present study was to preliminarily investigate in vitro, whether functional α7nAChR in adipocytes may suppress ASP‑induced inflammation and determine the possible signaling mechanism. Studies have reported associations between the expression of α7 nicotinic acetylcholine receptor (α7nAChR) and obesity, insulin resistance and diabetes. Additionally, α7nAChRs are important peripheral mediators of chronic inflammation, which is a key contributor to health problems in obesity. The primary aim of the present study was to evaluate the impact of exogenous ASP and α7nAChR on macrophage infiltration in adipose tissue and to examine the potential underlying molecular mechanism. Western blot analysis revealed that recombinant ASP increased the expression levels of monocyte chemoattractant protein‑1 (MCP‑1) and keratinocyte‑derived chemokine (KC) by 3T3‑L1 adipocytes. However, nicotine significantly inhibited the production of ASP‑induced cytokines via the stimulation of α7nAChR. It was also found that α7nAChR inhibited the ASP‑induced activation of p38 kinase and nuclear factor‑κB (NF‑κB), and the production of MCP‑1 and KC. These data indicated that α7nAChR caused the inhibition of ASP‑induced activation of p38 kinase and NF‑κB to inhibit the production of MCP‑1 and KC.
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October-2016
Volume 14 Issue 4

Print ISSN: 1791-2997
Online ISSN:1791-3004

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Spandidos Publications style
Jiao ZY, Wu J, Liu C, Wen B, Zhao WZ and Du XL: Nicotinic α7 receptor inhibits the acylation stimulating protein‑induced production of monocyte chemoattractant protein‑1 and keratinocyte‑derived chemokine in adipocytes by modulating the p38 kinase and nuclear factor‑κB signaling pathways. Mol Med Rep 14: 2959-2966, 2016
APA
Jiao, Z., Wu, J., Liu, C., Wen, B., Zhao, W., & Du, X. (2016). Nicotinic α7 receptor inhibits the acylation stimulating protein‑induced production of monocyte chemoattractant protein‑1 and keratinocyte‑derived chemokine in adipocytes by modulating the p38 kinase and nuclear factor‑κB signaling pathways. Molecular Medicine Reports, 14, 2959-2966. https://doi.org/10.3892/mmr.2016.5630
MLA
Jiao, Z., Wu, J., Liu, C., Wen, B., Zhao, W., Du, X."Nicotinic α7 receptor inhibits the acylation stimulating protein‑induced production of monocyte chemoattractant protein‑1 and keratinocyte‑derived chemokine in adipocytes by modulating the p38 kinase and nuclear factor‑κB signaling pathways". Molecular Medicine Reports 14.4 (2016): 2959-2966.
Chicago
Jiao, Z., Wu, J., Liu, C., Wen, B., Zhao, W., Du, X."Nicotinic α7 receptor inhibits the acylation stimulating protein‑induced production of monocyte chemoattractant protein‑1 and keratinocyte‑derived chemokine in adipocytes by modulating the p38 kinase and nuclear factor‑κB signaling pathways". Molecular Medicine Reports 14, no. 4 (2016): 2959-2966. https://doi.org/10.3892/mmr.2016.5630