title: Cross-talk between α7 nAChR-mediated cholinergic pathway and acylation stimulating protein signaling in 3T3-L1 adipocytes: role of NFκB and STAT3.
abstract: Inflammation is a key feature in adipose tissue, especially in association with obesity comorbidies. The novel adipokine acylation stimulating protein (ASP) is one factor implicated in the inflammatory response. The disruption of the α7 nicotine acetylcholine receptor (α7nAChR), an important component of the endogenous non-neural cholinergic defense system, may exacerbate sustained inflammatory phenotype. We examined cholinergic regulation of ASP-initiated inflammatory response in 3T3-L1 adipocytes. Our results show that preincubation of 3T3-L1 cells with α7nAChR agonist GTS-21 significantly reduces ASP-mediated chemokine MCP-1 secretion, which is regulated though nuclear factor κB (NFκB) and signal transducer and activator of transcription 3 (STAT3). Treatment of 3T3-L1 cells with GTS-21 significantly reduced NFκB activation by DNA binding and STAT3 activation by disturbing post-translational modification.
authors.affiliation: a Department of Pediatrics, First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China.
authors.forename: Jing
authors.initials: J
authors.lastname: Wu
authors.affiliation: b Department of Cardiovascular Surgery, First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China.
authors.forename: Zhou-yang
authors.initials: ZY
authors.lastname: Jiao
authors.affiliation: c Department of Histology & Embryology, College of Basic Medical Science, Zhengzhou University, Zhengzhou, 450001, China.
authors.forename: Zhe
authors.initials: Z
authors.lastname: Zhang
authors.affiliation: a Department of Pediatrics, First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China.
authors.forename: Zhi-hui
authors.initials: ZH
authors.lastname: Tang
authors.affiliation: d Department of Endocrinology, First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China.
authors.forename: Hao-hao
authors.initials: HH
authors.lastname: Zhang
authors.affiliation: e Department of Pediatrics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
authors.forename: Hui-ling
authors.initials: HL
authors.lastname: Lu
authors.affiliation: f Centre de Recherche Institut Universitaire de Cardiologie & Pneumologie de Québec, Université Laval, QC, G1V 4G5, Canada.
authors.forename: Katherine
authors.initials: K
authors.lastname: Cianflone
mesh_terms: D041721:3T3-L1 Cells; D017667:Adipocytes / Q000378:metabolism*; D000818:Animals; D018932:Chemokine CCL2 / Q000378:metabolism; D015926:Complement C3a / Q000378:metabolism*; D051379:Mice; D016328:NF-kappa B / Q000378:metabolism*; D050796:STAT3 Transcription Factor / Q000378:metabolism*; D015398:Signal Transduction; D064569:alpha7 Nicotinic Acetylcholine Receptor / Q000378:metabolism*
chemical_list: C491768:Ccl2 protein, mouse; D018932:Chemokine CCL2; D016328:NF-kappa B; D050796:STAT3 Transcription Factor; C494087:Stat3 protein, mouse; D064569:alpha7 Nicotinic Acetylcholine Receptor; C044541:complement C3a, des-Arg-(77)-; D015926:Complement C3a
keywords: acylation stimulating protein; adipocyte; inflammation; obesity; obésité; protéine de stimulation de l’acylation; récepteur nicotinique de l’acétycholine a7; α7 nicotine acetylcholine receptor