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首页> 外文期刊>Cellular Signalling >C5L2 and C5aR interaction in adipocytes and macrophages: Insights into adipoimmunology
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C5L2 and C5aR interaction in adipocytes and macrophages: Insights into adipoimmunology

机译：脂肪细胞和巨噬细胞中的C5L2和C5aR相互作用：脂肪免疫学的见解

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Obesity is associated with inflammation characterized by increased infiltration of macrophages into adipose tissue. C5aR-like receptor 2 (C5L2) has been identified as a receptor for acylation-stimulating protein (ASP) and the inflammatory factor C5a, which also binds C5aR. The present study examines the effects of ligands ASP and C5a on interactions between the receptors C5L2 and C5aR in 3T3-L1 adipocytes and J774 macrophages.BRET experiments indicate that C5L2 and C5aR form homo- and heterodimers in transfected HEK 293 cells, which were stable in the presence of ligand. Cell surface receptor levels of C5L2 and C5aR increased during 3T3-L1 adipocyte differentiation; both receptors are also highly expressed in J774 macrophages. Using confocal microscopy to evaluate endogenous receptors in adipocytes following stimulation with ASP or C5a, C5L2 is internalized with increasing perinuclear colocalization with C5aR. There is little C5a-dependent colocalization in macrophages. While adipocyte-conditioned medium (ACM) increased C5L2-C5aR colocalization in macrophages, this was blocked by C5a. ASP stimulation increased Akt (Ser473) phosphorylation in both cell types; C5a induced slight Akt phosphorylation in adipocytes with less effect in macrophages. ASP, but not C5a, increased fatty acid uptake/esterification in adipocytes.C5L2-C5aR homodimerization versus heterodimerization may thus contribute to differential responses obtained following ASP vs C5a stimulation of adipocytes and macrophages, providing new insights into the complex interaction between these two cell types within adipose tissue. Studying the mechanisms involved in the differential responses of C5L2-C5aR activation based on cell type will further our understanding of inflammatory processes in obesity.
机译：肥胖与炎症有关，炎症的特征在于巨噬细胞向脂肪组织的浸润增加。 C5aR样受体2（C5L2）已被鉴定为酰化刺激蛋白（ASP）和炎症因子C5a（也与C5aR结合）的受体。本研究探讨了配体ASP和C5a对3T3-L1脂肪细胞和J774巨噬细胞中受体C5L2和C5aR之间相互作用的影响.BRET实验表明C5L2和C5aR在转染的HEK 293细胞中形成同二聚体和异二聚体，在HEK 293细胞中稳定配体的存在。在3T3-L1脂肪细胞分化过程中，C5L2和C5aR的细胞表面受体水平增加。两种受体在J774巨噬细胞中也高度表达。使用共聚焦显微镜评估用ASP或C5a刺激后脂肪细胞中的内源性受体，C5L2被内化，并与C5aR的核周共定位增加。在巨噬细胞中几乎没有C5a依赖性共定位。虽然脂肪细胞条件培养基（ACM）可增加巨噬细胞中C5L2-C5aR的共定位作用，但C5a阻止了它的定位。 ASP刺激可增加两种细胞类型中的Akt（Ser473）磷酸化。 C5a诱导脂肪细胞中轻微的Akt磷酸化，而对巨噬细胞的影响较小。 ASP，而不是C5a，增加了脂肪细胞中脂肪酸的摄取/酯化作用.C5L2-C5aR同源二聚化与异源二聚化可能因此促进了ASP与C5a刺激脂肪细胞和巨噬细胞后获得的差异反应，从而为这两种细胞类型之间的复杂相互作用提供了新的见解在脂肪组织内。研究基于细胞类型的C5L2-C5aR激活的差异反应所涉及的机制，将进一步加深我们对肥胖中炎症过程的理解。

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