细胞内细胞激活的不同模式是由细胞外组织素和细菌性脂质聚合糖化物产生的
Sophia H Piffard1, Grant W Hennig, Adrian M Sackheim1
1Departments of Emergency Medicine.
Shock (Augusta, Ga.)
|August 28, 2024
概括
历史素,而不是LPS,在内皮细胞 (ECs) 中触发快速反应. 基质子在动脉和静脉中诱导了不同的信号模式,突出了差异性的EC激活机制.
科学领域:
- 细胞生物学 细胞生物学
- 血管生物学 血管生物学
- 免疫学 免疫学 免疫学
背景情况:
- 内皮细胞 (ECs) 响应创伤因素,如组织蛋白和败血症信号,如细菌脂多糖 (LPS) 与 (Ca 2+) 波动.
- 希斯顿与LPS之间的EC激活的独特模式和动力学仍然不清楚.
- 了解这些反应对于区分细胞对创伤和感染的反应至关重要.
研究的目的:
- 为了研究和比较Ca 2+响应的时空模式,在ECs中受激素和LPS刺激.
- 为了确定基因组是否在动脉和静脉内皮细胞中引起不同的Ca 2+信号模式.
- 探索LPS和基因素对EC Ca 2+活性和基因表达的联合作用.
主要方法:
- 在培养的EC (EA.hy926) 和来自小鼠动脉和静脉的本地EC中,对Ca 2+事件的高速活细胞成像.
- 通过激素或LPS单独或组合刺激,然后量化Ca 2+流行率.
- 经过6小时暴露于质子或LPS后,ECs的RNA测序.
主要成果:
- 基因组素在几秒钟内迅速增加了EC中的Ca 2+活性,而LPS的影响很小.
- 基因组激素在动脉和静脉中诱导了明显的,大型异常的Ca 2+事件,具有独特的时空模式 ('动脉中的红斑',静脉中的单个细胞反应).
- 前期暴露于LPS增强了基因素诱导的Ca 2+活性;这两种刺激都改变了基因表达,但诱导的mRNAs不同.
结论:
- 基因组和LPS通过不同的添加机制激活EC,基因组是唯一导致显著异常Ca2+事件的.
- 动脉和静脉EC表现出差异的时空Ca 2+对组织蛋白刺激的反应.
- 这些发现揭示了对创伤和败血症信号的特定细胞反应,影响了血管健康.
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