血管生成
Notch信号通路
基因敲除
心肌梗塞
心功能曲线
脐静脉
体内
信号转导
细胞生物学
细胞凋亡
医学
癌症研究
化学
内科学
内分泌学
生物
体外
心力衰竭
生物化学
生物技术
作者
Xueliang Zhou,Rongrong Zhu,Sheng Liu,Hua Xu,Xinping Xu,Qicai Wu,Ji‐chun Liu
摘要
Abstract Currently, the role of Notch signaling during myocardial infarction (MI) remains controversy. In this study we used in vitro and in vivo approaches to investigate the role of Notch signaling in MI. Using cultured human umbilical vein endothelial cells exposed to hypoxia/reoxygenation (H/R), we demonstrated that H/R inhibited the proliferation, VEGF secretion, and tube formation of HUVECs, and these effects were correlated with the inhibition of Notch signaling. Furthermore, these effects were antagonized by overexpression of NICD but aggravated by knockdown of NICD. In addition, in MI model rats we found that heart dysfunction and angiogenesis in model rats was partly improved by NICD overexpression but was aggravated by knockdown of NICD. In conclusion, these data demonstrate that Notch signaling is downregulated in H/R injury in the hearts. Artificial activation of Notch signaling could promote myocardial survival and angiogenesis and improve cardiac function following H/R injury.
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