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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Purinergic receptors modulate MAP kinases and transcription factors that control microglial inflammatory gene expression.
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Purinergic receptors modulate MAP kinases and transcription factors that control microglial inflammatory gene expression.

机译：嘌呤能受体调节MAP激酶和控制小神经胶质炎性基因表达的转录因子。

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摘要

Following many types of brain injury, microglial cell hyperactivation, and the subsequent release of neurotoxic mediators into the CNS contributes to inflammation and neuronal death. Among the proteins important for modulating the inflammatory function of microglia are the P2 purinergic receptors for which extracellular adenine nucleotides, such as ATP, are ligands. Because adenine nucleotides are abundant in the extracellular fluid following brain injury, ATP may represent an important component of the inflammatory microenvironment controlling microglial cell function. Although much work has been done examining the mechanisms whereby adenine nucleotides stimulate inflammatory mediator production, little is known concerning their complementary inhibitory effects. In this review we will focus on what is currently known about the microglial inhibitory effects of adenine nucleotides in the context of inflammation and summarize the current knowledge of their effects via purinergic receptors on microglial signal transduction pathways including transcription factors important for controlling inflammatory gene expression. The relevance of these mechanisms to microglial inflammatory function and physiology will be discussed. Further, we present data here illustrating that MAP kinase signal transduction pathways are altered in activated microglia that have been primed with or co-exposed to adenine nucleotides; effects that are stimulus- and MAPK pathway-specific. We also demonstrate the ability of P2X7 receptors to stimulate the phosphorylation of CREB, a putative inhibitory transcription factor in microglia. Together, these data indicate that ATP may be an endogenous inhibitor or neuroprotective molecule decreasing the inflammatory capacity of microglia.
机译：在许多类型的脑损伤之后，小胶质细胞过度活化，以及随后神经毒性介质释放到CNS中，导致炎症和神经元死亡。在对调节小胶质细胞的炎症功能重要的蛋白质中，有P2嘌呤能受体，其胞外腺嘌呤核苷酸（如ATP）是配体。由于脑损伤后细胞外液中腺嘌呤核苷酸丰富，ATP可能代表了控制微胶质细胞功能的炎症微环境的重要组成部分。尽管已经进行了大量工作来研究腺嘌呤核苷酸刺激炎症介质产生的机制，但对其互补的抑制作用知之甚少。在这篇综述中，我们将重点关注腺嘌呤核苷酸在炎症中对小胶质细胞的抑制作用的当前已知知识，并总结其通过嘌呤能受体对小胶质细胞信号转导途径的作用的当前知识，包括对控制炎症基因表达重要的转录因子。这些机制与小胶质细胞炎症功能和生理学的相关性将进行讨论。此外，我们在此处提供的数据说明，MAP激酶信号转导途径在已被腺嘌呤核苷酸引发或共同暴露于活化小胶质细胞中发生了改变;刺激和MAPK途径特定的作用。我们还证明了P2X7受体能够刺激小胶质细胞中一种假定的抑制性转录因子CREB的磷酸化。总之，这些数据表明ATP可能是减少小胶质细胞炎症能力的内源性抑制剂或神经保护分子。

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