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Related Collections Immunobiology Red Cells Gene Expression Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 15 February 2001, Vol. 97, No. 4, pp. 1009-1015 IMMUNOBIOLOGY Accumulation of HIF-1 under the influence of nitric oxide Katrin Britta Sandau, Joachim Fandrey, and Bernhard Brüne From the University of Erlangen-Nürnberg, Faculty of Medicine, Department of Medicine IVExperimental Division, and Nikolaus-Fiebiger Center, Clinical Project Group I, Erlangen, Germany; and the University of Essen, Institute of Physiology, Essen, Germany. The key player for adaptation to reduced oxygen availability is the transcription factor hypoxia-inducible factor 1 (HIF-1), composed of the redox-sensitive HIF-1 and the constitutively expressed HIF-1 subunits. Under normoxic conditions, HIF-1 is rapidly degraded, whereas hypoxia, CoCl2, or desferroxamine promote protein stabilization, thus evoking its transcriptional activity. Because HIF-1 is regulated by reactive oxygen species, investigation of the impact of reactive nitrogen species was intended. By using different nitric oxide (NO) donors, dose- and time-dependent HIF-1 accumulation in close correlation with the release of NO from chemically distinct NO donors was established. Intriguingly, small NO concentrations induced a faster but transient HIF-1 accumulation than higher doses of the same NO donor. In contrast, NO attenuated up-regulation of HIF-1 evoked by CoCl2 in a concentration- and time-dependent manner, whereas the desferroxamine-elicited HIF-1 signal remained unaltered. To demonstrate an autocrine or paracrine signaling function of NO, we overexpressed the inducible NO synthase and used a coculture system of activated macrophages and tubular cells. Expression of the NO synthase induced HIF-1 accumulation, which underscored the role of NO as an intracellular activator for HIF-1. In addition, macrophage-derived NO triggered HIF-1 up-regulation in LLC-PK1 target cells, which points to intercellular signaling properties of NO in achieving HIF-1 accumulation. Our results show that NO does not only modulate the HIF-1 response under hypoxic conditions, but it also functions as a HIF-1 inducer. We conclude that accumulation of HIF-1 occurs during hypoxia but also under inflammatory conditions that are characterized by sustained NO formation. © 2001 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: R. P. Rhoads, R. M. Johnson, C. R. Rathbone, X. Liu, C. Temm-Grove, S. M. Sheehan, J. B. Hoying, and R. E. Allen Satellite cell-mediated angiogenesis in vitro coincides with a functional hypoxia-inducible factor pathway Am J Physiol Cell Physiol, June 1, 2009; 296(6): C1321 - C1328. [Abstract] [Full Text] [PDF] J.-L. Balligand, O. Feron, and C. 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