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BioMed Research International
Volume 2017 (2017), Article ID 6895730, 13 pages
Research Article

Extracellular Signal-Regulated Kinase 5 is Required for Low-Concentration H2O2-Induced Angiogenesis of Human Umbilical Vein Endothelial Cells

1Department of Plastic and Reconstructive Surgery, Chinese PLA General Hospital, Beijing 100853, China
2Medicine School of Chinese PLA, Beijing 100853, China
3Department of General Surgery, Beijing Tongren Hospital, Capital Medical University, Beijing 100730, China
4Institute of Basic Medicine, Chinese PLA General Hospital, Beijing 100853, China
5Medicine School of Nankai University, Tianjin 300071, China

Correspondence should be addressed to Yan Han; moc.361@53368002731 and Weidong Han; moc.oohay@96wsrdwnah

Received 23 November 2016; Revised 22 February 2017; Accepted 9 March 2017; Published 30 April 2017

Academic Editor: Arianna Scuteri

Copyright © 2017 Shan Jiang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Background. The aim of this study was to assess the effects of low concentrations of H2O2 on angiogenesis of human umbilical vein endothelial cells (HUVECs) in vitro and explore the underlying mechanisms. Methods. HUVECs were cultured and stimulated with different concentrations of H2O2. Flow cytometric analysis was used to select an optimal concentration of H2O2 for the following experiments. Cell proliferation, migration, and tubule formation were evaluated by Cell Counting Kit-8 (CCK-8) assays, scratch wound assays, and Matrigel tubule formation assays, respectively. For gain and loss of function studies, constitutively active MEK5 (CA-MEK5) and ERK5 shRNA lentiviruses were used to activate or knock down extracellular signal-regulated kinase 5 (ERK5). Results. We found that low concentrations of H2O2 promoted HUVECs proliferation, migration, and tubule formation. ERK5 in HUVECs was significantly activated by H2O2. Enhanced ERK5 activity significantly amplified the proangiogenic effects of H2O2; in contrast, ERK5 knock-down abrogated the effects of H2O2. Conclusions. Our results confirmed that low concentrations of H2O2 promoted HUVECs angiogenesis in vitro, and ERK5 is an essential mediator of this process. Therefore, ERK5 may be a potential therapeutic target for promoting angiogenesis and improving graft survival.