1. Notch signaling promotes angiogenesis and improves cardiac function after myocardial infarction
- Author
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Xue-liang Zhou, Xinping Xu, Hua Xu, Rong-rong Zhu, Sheng Liu, Ji‐chun Liu, and Qi‐cai Wu
- Subjects
Male ,0301 basic medicine ,Cardiac function curve ,Angiogenesis ,Myocardial Infarction ,Notch signaling pathway ,Neovascularization, Physiologic ,Myocardial Reperfusion Injury ,Biochemistry ,Umbilical vein ,Rats, Sprague-Dawley ,03 medical and health sciences ,In vivo ,Human Umbilical Vein Endothelial Cells ,Animals ,Humans ,Medicine ,Molecular Biology ,Tube formation ,Gene knockdown ,Receptors, Notch ,business.industry ,Myocardium ,Cell Biology ,Hypoxia (medical) ,Rats ,Disease Models, Animal ,030104 developmental biology ,Cancer research ,medicine.symptom ,business ,Signal Transduction - 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.
- Published
- 2018
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