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Related Collections Hemostasis, Thrombosis, and Vascular Biology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, Vol. 95 No. 1 (January 1), 2000: pp. 189-197 Hypoxia response element of the human vascular endothelial growth factor gene mediates transcriptional regulation by nitric oxide: control of hypoxia-inducible factor-1 activity by nitric oxide Hideo Kimura, Alessandro Weisz, Yukiko Kurashima, Kouichi Hashimoto, Tsutomu Ogura, Fulvio D'Acquisto, Raffaelo Addeo, Masatoshi Makuuchi, and Hiroyasu Esumi From the Investigative Treatment Division, National Cancer Center Research Institute East, Kashiwa, Chiba, Japan; the Institute of General Pathology and Oncology, Second University of Naples, Naples, Italy; the Department of Experimental Pharmacology, University of Naples, Federico II, Naples, Italy; and the Second Department of Surgery, University of Tokyo, Tokyo, Japan. Nitric oxide (NO) regulates production of vascular endothelial growth factor (VEGF) by normal and transformed cells. We demonstrate that NO donors may up-regulate the activity of the human VEGF promoter in normoxic human glioblastoma and hepatoma cells independent of a cyclic guanosine monophosphate-mediated pathway. Deletion and mutation analysis of the VEGF promoter indicates that the NO-responsive cis-elements are the hypoxia-inducible factor-1 (HIF-1) binding site and an adjacent ancillary sequence that is located immediately downstream within the hypoxia-response element (HRE). This work demonstrates that the HRE of this promoter is the primary target of NO. In addition, VEGF gene regulation by NO, as well as by hypoxia, is potentiated by the AP-1 element of the gene. Our study also reveals that NO and hypoxia induce an increase in HIF-1 binding activity and HIF-1 protein levels, both in the nucleus and the whole cell. These results suggest that there are common features of the NO and hypoxic pathways of VEGF induction, while in part, NO mediates gene transcription by a mechanism distinct from hypoxia. This is demonstrated by a difference in sensitivity to guanylate cyclase inhibitors and a different pattern of HIF-1 binding. These results show that there is a primary role for NO in the control of VEGF synthesis and in cell adaptations to hypoxia. (Blood. 2000;95:189-197) CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: D. M. Birk, J. Barbato, L. Mureebe, and R. A. Chaer Basic Science Review: Current Insights on the Biology and Clinical Aspects of VEGF Regulation Vascular and Endovascular Surgery, December 1, 2009; 42(6): 517 - 530. [Abstract] [PDF] Y. Kuwano, A. Rabinovic, S. Srikantan, M. Gorospe, and B. 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