Adipose tissue complement factor B promotes adipocyte maturation
Adipose tissue complement factor B promotes adipocyte maturation
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DOI：
10.1016/j.bbrc.2017.11.069
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发表时间：
2018-01-01
影响因子：
3.1
通讯作者：
Nishimura, Fusanori
中科院分区：
文献类型：
--
作者：
Matsunaga, Hiroaki;Iwashita, Misaki;Nishimura, Fusanori
目的：众所周知，补体系统在宿主免疫中起着至关重要的作用。观察研究表明，补体系统相关分子，如补体因子B(CFB)和其他成分与肥胖和/或胰岛素抵抗参数相关。在本研究中，我们研究了脂肪细胞来源的CfB在脂肪组织代谢中的作用。方法：我们研究了脂肪细胞补体系统相关基因的表达水平。为了了解CFB在脂肪细胞中的作用，我们在3T3-L1前脂肪细胞中进行了CFB的过表达，并获得了脂肪细胞特异性的CFB转基因小鼠。结果：在内毒素刺激下，3T3-L1脂肪细胞与巨噬细胞共同培养后CFB的表达明显增强。在CFB过表达的细胞中，脂肪细胞分化/成熟相关基因的表达显著增强，编码PPAR-γ、脂肪细胞蛋白2和Perilipin。CFB转基因小鼠皮下脂肪组织中PPAR-γ、Perilipin、甾醇调节元件结合蛋白1c和CD36基因的表达显著增加。结论：CFB在脂肪细胞分化的晚期和随后的脂滴形成中起重要作用。(C)2017 Elsevier Inc.保留所有权利。
Objectives: It is well-known that the complement system plays an essential role in host immunity. Observational studies have indicated that complement system-related molecules such as complement factor B (CfB) and other components are correlated with obesity and/or insulin resistance parameters. In this study, we investigated the role of adipocyte-derived CfB in adipose tissue metabolism.Methods: We investigated the expression level of complement system-related genes in adipocytes. To understand the role of CfB in adipocyte, we performed Cfb overexpression in 3T3-L1 preadipocytes and generated adipocyte-specific Cfb transgenic mice.Results: Cfb expression was markedly enhanced in 3T3-L1 adipocytes co-cultured with macrophages following endotoxin stimulation. In Cfb-overexpressing cells, the expression of adipocyte differentiation/maturation-related genes encoding peroxisome proliferator-activated receptor gamma (Ppar gamma), adipocyte Protein 2 and perilipin was significantly enhanced. Cfb transgenic mice showed a marked increase in the expression of genes encoding Ppar gamma, perilipin, sterol regulatory element-binding protein 1 c, and Cd36 in the subcutaneous adipose tissue.Conclusions: CfB plays a crucial role in late-phase of adipocyte differentiation and subsequent lipid droplet formation. (C) 2017 Elsevier Inc. All rights reserved.