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Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
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Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
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相关实验视频

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An In Vitro Model of the Blood-brain Barrier Using Impedance Spectroscopy: A Focus on T Cell-endothelial Cell Interaction
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来自T淋巴细胞的脱落膜颗粒损害了内皮功能,并调节了内皮蛋白表达.

Sophie Martin1, Angela Tesse, Bénédicte Hugel

  • 1Pharmacologie et Physico-Chimie des Interactions Cellulaires et Moléculaires, UMR CNRS 7034, Faculté de Pharmacie, Illkirch, France.

Circulation
|March 17, 2004
PubMed
概括
此摘要是机器生成的。

来自T淋巴细胞的微粒 (MPs) 通过减少氧化 (NO) 和前环素通路来损害血管功能. 这些MPs改变内皮NO合成酶和caveolin-1表达,导致心血管并发症.

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科学领域:

  • 血管生物学 血管生物学
  • 细胞信号传输 细胞信号传输
  • 免疫学 免疫学 免疫学

背景情况:

  • 微粒 (MP) 是细胞激活过程中释放的前凝和前炎囊泡.
  • 来自T淋巴细胞的MPs与各种病理状况有关.

研究的目的:

  • 研究T淋巴细胞衍生MPs对血管内皮功能的影响.
  • 阐明MP诱导的内皮功能障碍背后的分子机制.

主要方法:

  • MPs是由人类T细胞系生成的.
  • 用小鼠的大动脉环和小介质动脉来评估血管反应.
  • 通过测量对乙胆和剪切应力的放松来评估内皮功能.
  • 分析了内皮NO合成酶 (eNOS) 和caveolin-1的蛋白质表达水平.

主要成果:

  • 来自T细胞的MPs损害了主动脉环中的乙胆诱导的放松和中枢动脉中剪切应激诱导的扩张.
  • 损伤涉及氧化 (NO) 和前环素通路的改变.
  • MP 效应归因于 eNOS 表达率下降和卡维奥林-1 表达率增加.
  • 糖尿病患者的MP和糖尿病患者或艾滋病毒感染患者的循环MP也减少了eNOS表达.

结论:

  • 来自T淋巴细胞的MPs在大动脉和小动脉中诱导内皮功能障碍.
  • 通过调节eNOS和caveolin-1表达,MPs改变了NO和前环素通路.
  • 这些发现增强了对循环MP在心血管和免疫疾病中的作用的理解.