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首页> 外文期刊>Cell cycle >Intracellular accumulation of cell cycle regulatory proteins and nucleolin re-localization are associated with pre-lethal ultrastructural lesions in circulating T lymphocytes: The HIV-induced cell cycle dysregulation revisited.
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Intracellular accumulation of cell cycle regulatory proteins and nucleolin re-localization are associated with pre-lethal ultrastructural lesions in circulating T lymphocytes: The HIV-induced cell cycle dysregulation revisited.

机译:细胞周期调节蛋白和核仁重新定位的细胞内积累与循环T淋巴细胞的致致致致致致致致致致致致致死的超微结构病变有关:艾滋病毒诱导的细胞周期失调再致讨。

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摘要

The HIV-induced demise of CD4-T cells is thought to be a result of the execution of genetically programmed cell death that occurs in lymphoid tissue, where many resident T cells are chronically hyperactivated. Since HIV-induced alterations of cell cycle control has been often indicated as prominent mechanism of immune hyper activation and cause of apoptotic death, the signal pathway involved in cell cycle dysregulation of T lymphocytes from HIV infected patients was extensively studied. Here, we also demonstrate that circulating T lymphocytes leave lymphoid tissues with diffused regressive lesions (vacuolization, blebbing, nuclear evanescence and organelle swelling). Equally diffused are biochemical anomalies that accompany the overall disarrangement of cell structure, particularly the fragmentation and diffusion into the cytoplasm of C23/nucleolin, the intracellular accumulation of short lived regulatory proteins and the decrease in expression of membrane proteins. All this is something more than a cell cycle-related remodelling of cell morphology and biochemical mechanisms, and rather recalls a necrotic/oncotic cell damage. Since these changes are associated with adaptive mechanisms to hypoxia, we give evidence for alteration of cell cycle control developing in conditions of scarce energy supply.
机译:CD4-T细胞的HIV诱导的消亡被认为是在淋巴组织中发生的转基因编程的细胞死亡的结果,其中许多驻留T细胞是长静动的。由于HIV诱导的细胞周期控制的改变通常被指示为免疫超激活和凋亡死因的突出机制,因此广泛地研究了来自HIV感染患者的T淋巴细胞的细胞周期失调的信号途径。在这里,我们还证明循环T淋巴细胞随着漫射厌恶滞后病变离开淋巴组织(真空化,膨胀,核缺陷和细胞器肿胀)。同样扩散是伴随细胞结构的整体脱离的生化异常,特别是C23 /核仁的细胞质的碎裂和扩散,短暂的调节蛋白的细胞内积累和膜蛋白表达的减少。所有这些都是细胞周期相关的细胞形态和生物化学机制的重塑,而且召回坏死/持续的细胞损伤。由于这些变化与对缺氧的自适应机制相关联,因此我们提供了在稀缺能量供应条件下改变细胞周期控制的改变。

著录项

  • 来源
    《Cell cycle》 |2010年第11期|共11页
  • 作者

    Piedimonte G;

  • 作者单位

    Department of Hygiene Public Health and Preventive Medicine University of Messina Messina Italy.;

  • 收录信息
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 细胞生物学;
  • 关键词

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