A20在心脏中被动态调节,并抑制了多变性反应
Stuart A Cook1, Mikhail S Novikov, Youngkeun Ahn
1Program in Cardiovascular Gene Therapy, Cardiovascular Research Centre and Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Charlestown, Mass 02129, USA.
Circulation
|August 6, 2003
概括
随着心脏应激,A20蛋白表达增加,通过阻断NF-kappaB信号传递来抑制心脏缩. 这种保护作用发生在不增加心肌细胞亡的情况下.
科学领域:
- 心血管生物学 心血管生物学
- 分子心脏病学分子心脏病学
- 细胞信号传递 细胞信号传递
背景情况:
- 核因子 (NF) -kappaB信号与心肌细胞缩有关.
- A20是已知的NF-kappaB信号传递的抑制剂.
研究的目的:
- 研究A20的心脏调节和生物活性.
- 确定A20在抑制心脏NF-kappaB信号传递中的作用.
主要方法:
- 在小鼠中进行大动脉带状检查,以评估A20表达.
- 刺激培养的新生儿心肌细胞与烯或内甲蛋白-1.
- 腺病毒载体介导的基因转移以表达心肌细胞中的A20或dnIKKbeta.
主要成果:
- 甲20mRNA在小鼠的前大动脉带带后显著上调,与NF-kappaB激活相关.
- A20的表达增加了心肌细胞刺激的高变性药物,并行NF-kappaB的激活.
- A20表达抑制了NF-kappaB信号传递和心肌细胞的高性反应,而不会增加亡.
结论:
- A20通过心脏中的急性生物力学压力来动态调节.
- 通过抑制NF-kappaB信号传递,A20可以减轻心脏缩.
- 在压力期间,A20保护心肌细胞免受亡.
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