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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.
 Previous Article | Table of Contents | Next Article 
HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY
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. N. Garcia, and
Gregg L. Semenza
From the Vascular Program, Institute for Cell Engineering; the Departments of Pediatrics, Medicine, Oncology, and Radiation Oncology; and the McKusick-Nathans Institute of Genetic Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD.
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 nonhypoxic versus hypoxic conditions and in nonhypoxic cells infected with adenovirus encoding beta-galactosidase versus a constitutively active form of HIF-1 (AdCA5). There were 245 gene probes that 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 down-regulated by both hypoxia and AdCA5 encoded proteins involved in cell growth/proliferation. Many genes up-regulated 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 nonhypoxic 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.
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T.-C. Chang, C.-J. Huang, K. Tam, S.-F. Chen, K. T. Tan, M.-S. Tsai, T.-N. Lin, and S.-K. Shyue
Stabilization of Hypoxia-inducible Factor-1{alpha} by Prostacyclin under Prolonged Hypoxia via Reducing Reactive Oxygen Species Level in Endothelial Cells
J. Biol. Chem.,
November 4, 2005;
280(44):
36567 - 36574.
[Abstract]
[Full Text]
[PDF]
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H. Y. Yeung, K. P. Lai, H. Y. Chan, N. K. Mak, G. F. Wagner, and C. K. C. Wong
Hypoxia-Inducible Factor-1-Mediated Activation of Stanniocalcin-1 in Human Cancer Cells
Endocrinology,
November 1, 2005;
146(11):
4951 - 4960.
[Abstract]
[Full Text]
[PDF]
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K. R. Stenmark and V. Balasubramaniam
Angiogenic Therapy for Bronchopulmonary Dysplasia: Rationale and Promise
Circulation,
October 18, 2005;
112(16):
2383 - 2385.
[Full Text]
[PDF]
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T. H. Patel, H. Kimura, C. R. Weiss, G. L. Semenza, and L. V. Hofmann
Constitutively active HIF-1{alpha} improves perfusion and arterial remodeling in an endovascular model of limb ischemia
Cardiovasc Res,
October 1, 2005;
68(1):
144 - 154.
[Abstract]
[Full Text]
[PDF]
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R. Bilton, N. Mazure, E. Trottier, M. Hattab, M.-A. Dery, D. E. Richard, J. Pouyssegur, and M. C. Brahimi-Horn
Arrest-defective-1 Protein, an Acetyltransferase, Does Not Alter Stability of Hypoxia-inducible Factor (HIF)-1{alpha} and Is Not Induced by Hypoxia or HIF
J. Biol. Chem.,
September 2, 2005;
280(35):
31132 - 31140.
[Abstract]
[Full Text]
[PDF]
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G. L. Semenza
Pulmonary Vascular Responses to Chronic Hypoxia Mediated by Hypoxia-inducible Factor 1
Proceedings of the ATS,
April 1, 2005;
2(1):
68 - 70.
[Abstract]
[Full Text]
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