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Editorial: an introduction and welcome to Hypoxia 编辑:介绍和欢迎缺氧
Pub Date : 2013-10-31 DOI: 10.2147/HP.S52866
D. Katschinski
License. The full terms of the License are available at http://creativecommons.org/licenses/by-nc/3.0/. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. Permissions beyond the scope of the License are administered by Dove Medical Press Limited. Information on how to request permission may be found at: http://www.dovepress.com/permissions.php Hypoxia 2013:1 29–30 Hypoxia Dovepress
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引用次数: 0
Prolyl-hydroxylase 3: Evolving Roles for an Ancient Signaling Protein. 脯氨酸羟化酶3:一种古老信号蛋白的进化作用。
Pub Date : 2013-10-01 DOI: 10.2147/HP.S50091
Trenton L Place, Frederick E Domann

The ability of cells to sense oxygen is a highly evolved process that facilitates adaptations to the local oxygen environment and is critical to energy homeostasis. In vertebrates, this process is largely controlled by three intracellular prolyl-4-hydroxylases (PHD 1-3). These related enzymes share the ability to hydroxylate the hypoxia-inducible transcription factor (HIF), and therefore control the transcription of genes involved in metabolism and vascular recruitment. However, it is becoming increasingly apparent that proline-4-hydroxylation controls much more than HIF signaling, with PHD3 emerging as an exceptionally unique and functionally diverse PHD isoform. In fact, PHD3-mediated hydroxylation has recently been purported to function in such diverse roles as sympathetic neuronal and muscle development, sepsis, glycolytic metabolism, and cell fate. PHD3 expression is also highly distinct from that of the other PHD enzymes, and varies considerably between different cell types and oxygen concentrations. This review will examine the evolution of oxygen sensing by the HIF-family of PHD enzymes, with a specific focus on complex nature of PHD3 expression and function in mammalian cells.

细胞感知氧气的能力是一个高度进化的过程,有助于适应局部氧气环境,对能量稳态至关重要。在脊椎动物中,这一过程主要由三种细胞内的4-羟化酶控制(PHD 1-3)。这些相关酶具有羟基化缺氧诱导转录因子(HIF)的能力,因此控制了参与代谢和血管募集的基因的转录。然而,脯氨酸-4-羟基化控制的不仅仅是HIF信号,PHD3作为一种非常独特和功能多样化的PHD亚型出现越来越明显。事实上,phd3介导的羟基化最近被认为在交感神经元和肌肉发育、败血症、糖酵解代谢和细胞命运等多种作用中起作用。PHD3的表达也与其他PHD酶高度不同,并且在不同的细胞类型和氧浓度之间变化很大。这篇综述将研究hif家族的PHD酶的氧感应进化,特别关注哺乳动物细胞中PHD3表达和功能的复杂性。
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引用次数: 36
Hypoxia Attenuates Purinergic P2X Receptor-Induced Inflammatory Gene Expression in Brainstem Microglia. 缺氧可减弱脑干小胶质细胞嘌呤能P2X受体诱导的炎症基因表达。
Pub Date : 2013-08-06 DOI: 10.2147/HP.S45529
Stephanie M C Smith, Gordon S Mitchell, Scott A Friedle, Christine M Sibigtroth, Stéphane Vinit, Jyoti J Watters

Hypoxia and increased extracellular nucleotides are frequently coincident in the brainstem. Extracellular nucleotides are potent modulators of microglial inflammatory gene expression via P2X purinergic receptor activation. Although hypoxia is also known to modulate inflammatory gene expression, little is known about how hypoxia or P2X receptor activation alone affect inflammatory molecule production in brainstem microglia, nor how hypoxia and P2X receptor signaling interact when they occur together. In this study, we investigated the ability of a brief episode of hypoxia (2hrs) in the presence and absence of the non-selective P2X receptor agonist 2'(3')-O-(4-benzoylbenzoyl)adenosine-5'-triphosphate (BzATP) to promote inflammatory gene expression in brainstem microglia in adult rats. We evaluated inducible nitric oxide synthase (iNOS), tumor necrosis factor alpha (TNFα) and interleukin-6 (IL-6) mRNA levels in immunomagnetically-isolated brainstem microglia. Whereas iNOS and IL-6 gene expression increased with hypoxia and BzATP alone, TNFα expression was unaffected. Surprisingly, BzATP-induced inflammatory effects are lost after hypoxia, suggesting that hypoxia impairs pro-inflammatory P2X receptor signaling. We also evaluated the expression of key P2X receptors activated by BzATP, namely P2X1, P2X4 and P2X7 receptors. Whereas hypoxia did not alter their expression, BzATP upregulated P2X4 and P2X7 mRNAs; these effects were ablated in hypoxia. Although both P2X4 and P2X7 receptor expression correlated with increased microglial iNOS and IL-6 levels in microglia from normoxic rats, in hypoxia, P2X7 only correlated with IL-6, and P2X4 correlated only with iNOS. In addition, correlations between P2X7 and P2X4 were lost following hypoxia, suggesting that P2X4 and P2X7 receptor signaling differs in normoxia and hypoxia. Together, these data suggest that hypoxia suppresses P2X receptor-induced inflammatory gene expression, indicating a potentially immunosuppressive role of extracellular nucleotides in brainstem microglia following exposure to hypoxia.

脑干缺氧和细胞外核苷酸增加经常同时发生。细胞外核苷酸是通过P2X嘌呤能受体激活的小胶质炎症基因表达的有效调节剂。虽然缺氧也可以调节炎症基因表达,但对于单独缺氧或P2X受体激活如何影响脑干小胶质细胞中炎症分子的产生,以及当缺氧和P2X受体信号同时发生时如何相互作用,我们知之甚少。在这项研究中,我们研究了在存在和不存在非选择性P2X受体激动剂2'(3')- o -(4-苯甲酰基苯甲酰基)腺苷-5'-三磷酸(BzATP)的情况下短暂缺氧(2小时)促进成年大鼠脑干小胶质细胞炎症基因表达的能力。我们评估了诱导型一氧化氮合酶(iNOS)、肿瘤坏死因子α (TNFα)和白细胞介素6 (IL-6) mRNA在免疫磁分离脑干小胶质细胞中的表达水平。而iNOS和IL-6基因表达随缺氧和BzATP单独升高,tnf - α表达不受影响。令人惊讶的是,bzatp诱导的炎症效应在缺氧后消失,这表明缺氧会损害促炎P2X受体信号传导。我们还评估了BzATP激活的关键P2X受体,即P2X1, P2X4和P2X7受体的表达。而缺氧不改变它们的表达,BzATP上调P2X4和P2X7 mrna;这些作用在缺氧条件下消失。虽然P2X4和P2X7受体表达与正常缺氧大鼠小胶质细胞iNOS和IL-6水平升高相关,但在缺氧情况下,P2X7仅与IL-6相关,P2X4仅与iNOS相关。此外,P2X7和P2X4之间的相关性在缺氧后消失,这表明P2X4和P2X7受体信号在常氧和缺氧时是不同的。总之,这些数据表明缺氧抑制P2X受体诱导的炎症基因表达,表明暴露于缺氧后脑干小胶质细胞中细胞外核苷酸可能具有免疫抑制作用。
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引用次数: 14
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Hypoxia (Auckland, N.Z.)
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