期刊
JOURNAL OF CELLULAR BIOCHEMISTRY
卷 119, 期 8, 页码 7105-7112出版社
WILEY
DOI: 10.1002/jcb.27032
关键词
angiogenesis; hypoxia; reoxygenation; myocardial infarction; NICD; Notch
资金
- National Natural Science Foundation of China [81460065, 81570262]
- Natural Science Foundation of Jiangxi Province [20142BAB205039, 20152ACB20026]
- Jiangxi Provincial Universities Science Technology Floor Plan [KJLD1401]
- Jiangxi Provincial Department of Education Science and Technology Research Project [GJJ14004]
- Gan Po Talent 555 Program
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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