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MEK1-ERK2信号通路在体内保护心肌免受缺血性损伤
Daniel J Lips1, Orlando F Bueno, Benjamin J Wilkins
1Department of Cardiology, Maastricht University, and Heart Lung Center Utrecht, Maastricht and Utrecht, Netherlands.
Circulation
|April 21, 2004
概括
细胞外信号调节激酶1/2 (ERK1/2) 信号传递对于保护心脏免受因缺血-再输血损伤引起的损伤至关重要. 减少ERK2信号增加心脏损伤,而增强的信号提供保护.
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
- 信号传输 信号传输
背景情况:
- 心肌梗塞导致不可逆转的心肌细胞损失,导致心力衰竭.
- 线素激活蛋白激酶 (MAPK) 途径是心脏肌细胞死亡的关键在缺血-再输液期间.
- 细胞外信号调节激酶1/2 (ERK1/2) 的激活与心脏保护有关,通过对抗亡.
研究的目的:
- 确定ERK1/2信号在心脏保护中的因果作用,以防止缺血-再输血损伤.
- 研究调节MEK1-ERK1/2通路活性对心脏功能和存活率的体内影响.
主要方法:
- 对基因向小鼠进行分析,这些小鼠的Erk1和Erk2表达发生了变化 (Erk1无,Erk2异).
- 使用转基因小鼠在心脏中激活MEK1-ERK1/2信号.
- 评估心肌梗塞的大小,DNA碎片化 (梯级) 和TUNEL染色后缺血-再输血.
- 使用压力-体积循环记录评估心脏血液动力学功能.
主要成果:
- 转基因MEK1-ERK1/2小鼠表现出对缺血-再输液损伤的抵抗力.
- 埃尔克2+/-小鼠的发作区域显著扩大,DNA损伤标志物增加.
- 增强的MEK1-ERK1/2信号防止了DNA碎片化,并保留了血液动力学功能.
结论:
- 这项研究提供了第一个体内证据,表明ERK2信号对心肌保护至关重要.
- ERK2信号传递在减轻缺血-再输血事件后的心脏损伤方面发挥着至关重要的作用.
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