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. 2016 Jul 8;6:29417. doi: 10.1038/srep29417

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Copyright © 2016, Macmillan Publishers Limited

This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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VEGF treatment of endothelial cells activates HO-1-dependent migration, proliferation and angiogenesis in vitro and in vivo. Microarray and proteomic analyses revealed cyclin A1, cyclin E1 and vimentin as downstream targets of HO-1. VEGF induced an HO-1-dependent increase in cdk2 kinase and calpain activity. These changes increased cell cycle progression and vimentin cleavage respectively. The role of HO-1 was established using specific siRNAs and HO-1 agonists. Similarly the importance of both cyclin A1 and vimentin in pro-angiogenic effects of VEGF and HO-1 activity were demonstrated by cyclin A1 and vimentin gene silencing.