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鉴定了一种新型的氧化还原敏感基因Id3,该基因调解血管激素II诱导的细胞生长

Cornelius Mueller¹, Stephanie Baudler, Hilke Welzel

¹Klinik und Poliklinik Innere Medizin III, Universität des Saarlandes, Homburg, Germany.

|May 22, 2002

概括

ангиотензин II (Ang II) 通过超氧化物生产引起血管光滑肌肉细胞 (VSMC) 增殖,从而上调Id3. 抑制Id3阻断了这种生长,揭示了细胞控制中的新型氧化还原敏感途径.

科学领域:

心血管生物学心血管生物学
分子生物学分子生物学
细胞信号传输细胞信号传输

背景情况:

反应性氧物种 (ROS),特别是超氧化物 (O(2) ((-),都与细胞异常生长有关.
ангиотензин II (Ang II) 是血管氧化应激的一个关键诱导因子.
血管平滑肌细胞 (VSMC) Ang II诱导的增殖机制尚未完全理解.

研究的目的:

阐明Ang II诱导的VSMC增殖背后的分子机制.
识别参与VSMC生长控制的新型氧化还原敏感基因.

主要方法:

用Ang II或丁/丁氧化酶 (X/XO) 治疗VSMC,以诱导氧化应激.
用差异显示来分析基因表达.
使用了基因沉默 (反意义Id3) 和过度表达 (意义Id3).
评估了细胞循环调节者的蛋白质水平 (p21,p27,p53) 和视网母细胞瘤蛋白质酸化.

主要成果:

格II和X/XO刺激了VSMC的DNA合成和扩散.
一个新的氧化还原敏感基因Id3被确定并通过AngII和X/XO进行上调.
超氧化物脱酶,但不是酶,抑制了Id3的上调.
反感Id3消除了Ang II和X/XO诱导的VSMC扩散.
格II和Id3调节了p21 ((WAF1/Cip1),p27 ((Kip1) 和p53的表达,以及视网母细胞瘤蛋白酸化.

结论:

安格II通过超氧化物生产和随后的Id3上调促进VSMC的扩散.
Id3在调节下游细胞循环蛋白 (p21,p27,p53) 中起着至关重要的作用.
这项研究揭示了一种新的氧化还原敏感途径,可以控制血管系统中的细胞生长.

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