Notch signaling activation contributes to cardioprotection provided by ischemic preconditioning and postconditioning.
Notch signaling activation contributes to cardioprotection provided by ischemic preconditioning and postconditioning.
复制标题
Notch 信号激活有助于缺血预处理和后处理提供的心脏保护
DOI：
10.1186/1479-5876-11-251
复制
发表时间：
2013-10-08
影响因子：
7.4
通讯作者：
Liu JC
中科院分区：
文献类型：
--
作者：
Zhou XL;Wan L;Xu QR;Zhao Y;Liu JC
已知Notch信号在心肌缺血后被激活，但其在缺血预适应(IPC)和缺血后适应(IPost)提供的心脏保护中的作用尚不清楚。构建慢病毒载体，在H9c2心肌细胞和缺血再灌注损伤(IRI)、IPC或IPost损伤的大鼠心脏中过表达或敲除N1ICD。NOTCH1信号在心肌IPC和IPost过程中被激活，并可提高细胞活力和抑制细胞凋亡。此外，激活的Notch1信号稳定了线粒体膜电位，减少了IRI诱导的氧自由基。Notch1活化信号的心肌保护作用类似于IPC和IPost，这与STAT3的激活和对凋亡相关蛋白的调控有关。此外，在Langendorff心脏灌流模型中，激活的Notch1信号可恢复心肌缺血后的心功能，减少乳酸脱氢酶的释放，限制心肌梗死范围。结论：NOTCH1信号被激活，并介导IPC和IPost提供的心脏保护。NOTCH1信号可能代表了一种潜在的新的药物模拟物，用于缺血性心脏病的心脏保护。
Notch signaling is known to be activated following myocardial ischemia, but its role in cardioprotection provided by ischemic preconditioning (IPC) and ischemic postconditioning (IPost) remains unclear. Lentiviral vectors were constructed to overexpress or knockdown N1ICD in H9c2 cardiomyocyte and rat heart exposed to ischemia reperfusion injury (IRI), IPC or IPost. Notch1 signaling was activated during myocardial IPC and IPost, and could enhance cell viability and inhibit apoptosis. Furthermore, activated Notch1 signaling stabilized mitochondrial membrane potential and reduced reactive oxygen species induced by IRI. The cardioprotection provided by activated Notch1 signaling resembled that of IPC and IPost, which was related to Stat3 activation and regulation of apoptosis related proteins. Furthermore, in langendorff heart perfusion model, activated Notch1 signaling restored cardiac function, decreased lactate dehydrogenase release and limited infarct size after myocardial ischemia. Conclusions: Notch1 signaling is activated and mediates cardioprotection provided by IPC and Ipost. Notch1 signaling may represent a potential new pharmacologic mimic for cardioprotection of ischemic heart disease.
登录
查看更多内容
经典Notch通路通过JAK2/STAT3信号传导抑制活性氧的产生，保护小鼠肝细胞免受缺血/再灌注损伤
影响因子：
13.5
作者：
Yu, Heng-Chao;Qin, Hong-Yan;Han, Hua
通讯作者：
Han, Hua
影响因子：
2.9
作者：
Givogri, MI;de Planell, M;Bongarzone, ER
通讯作者：
Bongarzone, ER
Notch 激活静止心肌细胞的细胞周期重入和进展。
DOI：
10.1083/jcb.200806104
发表时间：
2008-10-06
期刊：
The Journal of cell biology
影响因子：
--
作者：
Campa VM;Gutiérrez-Lanza R;Cerignoli F;Díaz-Trelles R;Nelson B;Tsuji T;Barcova M;Jiang W;Mercola M
通讯作者：
Mercola M
影响因子：
4
作者：
Gao, Feng;Yao, Min;Duan, Huijun
通讯作者：
Duan, Huijun
Notch1 信号传导刺激未成熟心肌细胞的增殖。
DOI：
10.1083/jcb.200806091
发表时间：
2008-10-06
期刊：
The Journal of cell biology
影响因子：
--
作者：
Collesi C;Zentilin L;Sinagra G;Giacca M
通讯作者：
Giacca M