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首页> 外文期刊>Cell & Bioscience >Macrophages inhibit adipogenic differentiation of adipose tissue derived mesenchymal stem/stromal cells by producing pro-inflammatory cytokines
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Macrophages inhibit adipogenic differentiation of adipose tissue derived mesenchymal stem/stromal cells by producing pro-inflammatory cytokines

机译：巨噬细胞通过产生促炎细胞因子来抑制脂肪组织衍生的间充质茎/基质细胞的脂肪切分化

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Mesenchymal stem/stromal cells (MSCs) and macrophages are critical components in many tissue microenvironments, including that in adipose tissue. The close interaction between MSCs and macrophages modulates various adipose-related disease development. However, the effects of macrophages on the fate of MSCs remain largely elusive. We here studied the effect of macrophages on the adipogenic differentiation of MSCs. Macrophages were obtained from THP-1 cells treated with phorbol-12-myristate-13-acetate (PMA). The induced matured macrophages were then induced to undergo classically activated macrophage (M1) or alternatively activated macrophage (M2) polarization with Iipopolysaccharide (LPS)/interferon (IFN)-γ and interleukin (IL)-4/IL-13, respectively. The supernatants derived from macrophages under different conditions were applied to cultured human adipose tissue-derived mesenchymal stem/stromal cells (hADSCs) undergoing adipogenic differentiation. Adipogenic differentiation was evaluated by examining Oil Red O staining of lipid droplets and the expression of adipogenesis-related genes with real-time quantitative polymerase chain reaction (Q-PCR) and western blot analysis. The adipogenic differentiation of hADSCs was impaired when treated with macrophage-derived supernatants, especially that from the M1-polarized macrophage (M1-sup). The inhibitory effect was found to be mediated by the inflammatory cytokines, mainly tumor necrosis factor-α (TNF-α) and IL-1β. Blocking TNF-α and IL-1β with neutralizing antibodies partially alleviated the inhibitory effect of M1-sup. Macrophage-derived supernatants inhibited the adipogenic differentiation of hADSCs in vitro, irrespective of the polarization status (M0, M1 or M2 macrophages). M1-sup was more potent because of the higher expression of pro-inflammatory cytokines. Our findings shed new light on the interaction between hADSCs and macrophages and have implications in our understanding of disrupted adipose tissue homeostasis under inflammation.
机译：间充质茎/基质细胞（MSCs）和巨噬细胞是许多组织微环境中的关键组分，包括在脂肪组织中。 MSCs和巨噬细胞之间的密切相互作用调节了各种脂肪相关的疾病发展。然而，巨噬细胞对MSC的命运的影响仍然很大程度上是难以捉摸的。我们在这里研究了巨噬细胞对MSCs脂肪生成分化的影响。从用Phorbol-12- myristerate-13-乙酸盐（PMA）处理的THP-1细胞获得巨噬细胞。然后诱导诱导的成熟的巨噬细胞分别用IIPopolysaccharide（LPS）/干扰素（IFN）-γ和白细胞介素（IL）-4 / IL-13进行经典活化的巨噬细胞或可选地活化的巨噬细胞（M2）偏振。在不同条件下衍生自巨噬细胞的上清液被应用于培养的人脂肪组织衍生的间充质茎/基质细胞（HADSCs）经受脂肪分化的培养。通过检查脂液滴的油红O染色和利用实时定量聚合酶链反应（Q-PCR）和Western印迹分析来评估脂肪发生分化。当用巨噬细胞衍生的上清液处理时，尤其是从M1偏振巨噬细胞（M1-SUP）处理时，HADSCs的脂肪生成分化损害。发现抑制效果被炎性细胞因子介导，主要是肿瘤坏死因子-α（TNF-α）和IL-1β。阻断具有中和抗体的TNF-α和IL-1β部分缓解了M1-SUP的抑制作用。巨噬细胞衍生的上清液在体外抑制HADSCs的脂肪生成分化，而不管偏振状态（M0，M1或M2巨噬细胞）。由于促炎细胞因子的表达更高，M1-SUP更有效。我们的研究结果揭示了哈斯克斯毒素和巨噬细胞之间的相互作用，并对我们对炎症下破坏的脂肪组织稳态造成影响。

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