title: 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.
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.
authors: Department of Cardiovascular Surgery, First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, P.R. China.
authors: Zhou-Yang
authors: ZY
authors: Jiao
authors: Department of Pediatrics, First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, P.R. China.
authors: Jing
authors: J
authors: Wu
authors: Department of Cardiovascular Surgery, First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, P.R. China.
authors: Chao
authors: C
authors: Liu
authors: Department of Cardiovascular Surgery, First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, P.R. China.
authors: Bing
authors: B
authors: Wen
authors: Department of Cardiovascular Surgery, First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, P.R. China.
authors: Wen-Zeng
authors: WZ
authors: Zhao
authors: Department of Cardiovascular Surgery, Xiehe Hospital, Huazhong University of Science and Technology, Wuhan, Hubei 430022, P.R. China.
authors: Xin-Ling
authors: XL
authors: Du
mesh_terms: D041721:3T3-L1 Cells; D017667:Adipocytes / Q000166:cytology / Q000276:immunology*; D000818:Animals; D018932:Chemokine CCL2 / Q000276:immunology*; D018925:Chemokines / Q000276:immunology*; D015926:Complement C3a / Q000276:immunology*; D007249:Inflammation / Q000276:immunology; D020935:MAP Kinase Signaling System; D051379:Mice; D016328:NF-kappa B / Q000276:immunology*; D009765:Obesity / Q000276:immunology; D015398:Signal Transduction; D064569:alpha7 Nicotinic Acetylcholine Receptor / Q000276:immunology*
chemical_list: C491768:Ccl2 protein, mouse; D018932:Chemokine CCL2; D018925:Chemokines; D016328:NF-kappa B; D064569:alpha7 Nicotinic Acetylcholine Receptor; C044541:complement C3a, des-Arg-(77)-; C074302:keratinocyte-derived chemokines; D015926:Complement C3a