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Blood, 15 January 2005, Vol. 105, No. 2, pp. 659-669. Prepublished online as a Blood First Edition Paper on September 16, 2004; DOI 10.1182/blood-2004-07-2958. This Article Full Text (PDF) Supplemental Tables All Versions of this Article: 2004-07-2958v1 105/2/659    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Manalo, D. J Articles by Semenza, G. L Search for Related Content PubMed PubMed Citation Articles by Manalo, D. J Articles by Semenza, G. L Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted July 30, 2004 Accepted September 1, 2004 Transcriptional regulation of vascular endothelial cell responses to hypoxia by HIF-1 Dominador J Manalo, Ashley Rowan, Tera Lavoie, Lakshmi Natarajan, Brian D Kelly, Shui Q Ye, Joe G Garcia, and Gregg L Semenza* Vascular Program, Institute for Cell Engineering, Departments of Pediatrics, Medicine, Oncology, Radiation Oncology, and Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA * Corresponding author; email: gsemenza{at}jhmi.edu. Hypoxia-inducible factor 1 (HIF-1) activates transcription of genes encoding angiogenic growth factors, which are secreted by hypoxic cells and stimulate endothelial cells, leading to angiogenesis. To determine whether HIF-1 also mediates cell-autonomous responses to hypoxia, we have compared gene expression profiles in arterial endothelial cells cultured under non-hypoxic vs hypoxic conditions and in non-hypoxic cells infected with adenovirus encoding beta-galactosidase vs a constitutively-active form of HIF-1 (AdCA5). 245 gene probes showed at least 1.5-fold increase in expression in response to hypoxia and in response to AdCA5. 325 gene probes showed at least 1.5-fold decrease in expression in response to hypoxia and in response to AdCA5. The largest category of genes downregulated by both hypoxia and AdCA5 encoded proteins involved in cell growth/proliferation. Many genes upregulated by both hypoxia and AdCA5 encoded cytokines/growth factors, receptors, and other signaling proteins. Transcription factors accounted for the largest group of HIF-1-regulated genes, indicating that HIF-1 controls a network of transcriptional responses to hypoxia in endothelial cells. Infection of endothelial cells with AdCA5 under non-hypoxic conditions was sufficient to induce increased basement membrane invasion and tube formation similar to the responses induced by hypoxia, indicating that HIF-1 mediates cell-autonomous activation of endothelial cells. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: L. Martorell, M. Gentile, J. Rius, C. Rodriguez, J. Crespo, L. Badimon, and J. Martinez-Gonzalez The Hypoxia-Inducible Factor 1/NOR-1 Axis Regulates the Survival Response of Endothelial Cells to Hypoxia Mol. Cell. Biol., November 1, 2009; 29(21): 5828 - 5842. [Abstract] [Full Text] [PDF] G. L. Semenza Involvement of oxygen-sensing pathways in physiologic and pathologic erythropoiesis Blood, September 3, 2009; 114(10): 2015 - 2019. [Abstract] [Full Text] [PDF] A. GIATROMANOLAKI, A. FISKA, D. PITSIAVA, G. KARTALIS, M. I. KOUKOURAKIS, and E. 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