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首页> 外文期刊>Cytokine >Regulation of ADAMTS-1, -4 and -5 expression in human macrophages: Differential regulation by key cytokines implicated in atherosclerosis and novel synergism between TL1A and IL-17
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Regulation of ADAMTS-1, -4 and -5 expression in human macrophages: Differential regulation by key cytokines implicated in atherosclerosis and novel synergism between TL1A and IL-17

机译：人巨噬细胞中的Adamts-1，-4和-5表达：关键细胞因子涉及动脉粥样硬化和TL1A和IL-17之间的新型协同作用的差异调节

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Atherosclerosis is an inflammatory disease of the vasculature regulated by cytokines. Macrophages play a crucial role at all stages of this disease, including regulation of foam cell formation, the inflammatory response and stability of atherosclerotic plaques. For example, matrix metalloproteinases produced by macrophages play an important role in modulating plaque stability. More recently, the ADAMTS proteases, which are known to play a key role in the control of cartilage degradation during arthritis, have been found to be expressed in atherosclerotic lesions and suggested to have potentially important functions in the control of plaque stability. Unfortunately, the action of cytokines on the expression of ADAMTS family in macrophages is poorly understood. We have investigated the effect of classical cytokines (IFN-γ and TGF-β) and those that have been recently identified (TL1A and IL-17) on the expression of ADAMTS-1, -4 and -5 in human macrophages. The expression of all three ADAMTS members was induced during differentiation of monocytes into macrophages. TGF-β had a differential action with induction of ADAMTS-1 and -5 expression and attenuation in the levels of ADAMTS-4. In contrast, IFN-γ suppressed the expression of ADAMTS-1 without having an effect on ADAMTS-4 and -5. Although TL-1A or IL-17A alone had little effect on the expression of all the members, they induced their expression synergistically when present together. These studies provide new insight into the regulation of key ADAMTS family members in human macrophages by major cytokines in relation to atherosclerosis.
机译：动脉粥样硬化是由细胞因子调节的脉管系统的炎症性疾病。巨噬细胞在这种疾病的所有阶段发挥着至关重要的作用，包括调节泡沫细胞形成，动脉粥样硬化斑块的炎症反应和稳定性。例如，通过巨噬细胞产生的基质金属蛋白酶在调节斑块稳定性方面发挥着重要作用。最近，已知在关节炎期间对软骨降解进行关键作用的Adamts蛋白酶在动脉粥样硬化病变中表达，并建议在控制斑块稳定性方面具有潜在的重要功能。不幸的是，细胞因子对巨噬细胞中Adamts家族表达的作用很差。我们已经研究了经典细胞因子（IFN-γ和TGF-β）的效果，并且最近被鉴定（TL1A和IL-17）对人巨噬细胞中的Adamts-1，-4和-5的表达的影响。在将单核细胞的分化过程中诱导所有三个Adamts成员的表达到巨噬细胞期间。 TGF-β具有诱导Adamts-1和-5表达和衰减在Adamts-4水平中的差异作用。相反，IFN-γ抑制了Adamts-1的表达而不对Adamts-4和-5具有效果。虽然单独的TL-1A或IL-17A对所有构件的表达几乎没有影响，但它们在一起时协同诱导它们的表达。这些研究通过关于动脉粥样硬化的主要细胞因子，对人类巨噬细胞的重点进行了新的洞察力。

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