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氧化应激通过抑制内皮转录因子ERG的抑制诱导E-选择素表达
Jinjin Zhang1, Shuo Zhang1, Shanhu Xu1
1Medical Research Center, Shandong Provincial Qianfoshan Hospital, Shandong University, Jinan, China.
Journal of immunology (Baltimore, Md. : 1950)
|November 6, 2023
概括
内皮转录因子ETS相关基因 (ERG) 抑制了E-选择素基因转录. ERG抑制氧化应激诱导的内皮细胞粘附,为血栓形成提供了一个新的治疗点.
科学领域:
- 内皮细胞生物学 内皮细胞生物学
- 血栓形成的分子机制
- 在氧化应激中基因调节.
背景情况:
- 氧化应激通过增加内皮粘附来促进前血栓状况.
- 电选择蛋白是一种关键的内皮粘附分子,也是静脉血栓症的治疗标.
- 对于E-选择蛋白表达的调节机制的理解尚不完全.
研究的目的:
- 研究ETS相关基因 (ERG) 在调节E-选择素表达中的作用.
- 阐明ERG影响E-选择素转录和内皮粘附的机制.
- 为了确定ERG在E-选择素调节和血栓形成中的体内相关性.
主要方法:
- 在实验室中使用HUVECs治疗H2O2,RNA干扰和等离子体转染的研究.
- 在体内研究使用BALB/c小鼠接受过低酸治疗和Erg基因被删除的小鼠.
- 染色体免疫沉,光酶记者测定,并捕获高通量染色体构造捕获.
主要成果:
- 在HUVEC和小鼠模型中,H2O2治疗增加了E-选择蛋白,并降低了ERG表达.
- 在ERG Knockdown中,E-selectin的调节升高,而ERG过度表达则降低了它的调节.
- ERG直接与E-选择素促进体结合并抑制其活性,减少单细胞粘附.
结论:
- ERG作为一种抑制E-选择素基因转录的抑制剂.
- ERG在抑制氧化应激诱导的内皮细胞粘附方面发挥着至关重要的作用.
- 向ERG可能为预防血栓形成提供了一种新的治疗策略.
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