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Vol. 15, No. 19, pp. 2520-2532, October 1, 2001
1 Cancer Genetics Program and 2 Genome Analysis
Core Facility, UCSF Comprehensive Cancer Center,
3 Department of Anatomy and Cardiovascular Research
Institute, and 4 Department of Surgery, University of
California, San Francisco, San Francisco, California 94143, USA;
5 Regeneron Pharmaceuticals, Inc., Tarrytown, New York 10591, USA; 6 Laboratory of Human Carcinogenesis, National Cancer
Institute, National Institutes of Health, Bethesda, Maryland
20892-4255, USA; 7 Biology Department, University of
California, San Diego, La Jolla, California 92093-0346, USA
Hypoxia-inducible factor-1
(HIF-1) transactivates genes
required for energy metabolism and tissue perfusion and is necessary for embryonic development and tumor explant growth. HIF-1 is overexpressed during carcinogenesis, myocardial infarction, and wound
healing; however, the biological consequences of HIF-1 overexpression are unknown. Here, transgenic mice expressing
constitutively active HIF-1 in epidermis displayed a 66% increase
in dermal capillaries, a 13-fold elevation of total vascular
endothelial growth factor (VEGF) expression, and a six- to ninefold
induction of each VEGF isoform. Despite marked induction of
hypervascularity, HIF-1 did not induce edema, inflammation, or
vascular leakage, phenotypes developing in transgenic mice
overexpressing VEGF cDNA in skin. Remarkably, blood vessel leakage
resistance induced by HIF-1 overexpression was not caused by
up-regulation of angiopoietin-1 or angiopoietin-2. Hypervascularity
induced by HIF-1 could improve therapy of tissue ischemia.
[Key Words:
Hypoxia; HIF-1; angiogenesis; skin; epidermis; keratin]
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