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Research Article Free access | 10.1172/JCI119069

In vivo angiogenic activity and hypoxia induction of heterodimers of placenta growth factor/vascular endothelial growth factor.

Y Cao, P Linden, D Shima, F Browne, and J Folkman

Department of Surgery, Harvard Medical School, Boston, Massachusetts 02115, USA.

Find articles by Cao, Y. in: PubMed | Google Scholar

Department of Surgery, Harvard Medical School, Boston, Massachusetts 02115, USA.

Find articles by Linden, P. in: PubMed | Google Scholar

Department of Surgery, Harvard Medical School, Boston, Massachusetts 02115, USA.

Find articles by Shima, D. in: PubMed | Google Scholar

Department of Surgery, Harvard Medical School, Boston, Massachusetts 02115, USA.

Find articles by Browne, F. in: PubMed | Google Scholar

Department of Surgery, Harvard Medical School, Boston, Massachusetts 02115, USA.

Find articles by Folkman, J. in: PubMed | Google Scholar

Published December 1, 1996 - More info

Published in Volume 98, Issue 11 on December 1, 1996
J Clin Invest. 1996;98(11):2507–2511. https://doi.org/10.1172/JCI119069.
© 1996 The American Society for Clinical Investigation
Published December 1, 1996 - Version history
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Abstract

To investigate the in vivo angiogenic activity of placenta growth factor (PIGF) and its heterodimers with vascular endothelial growth factor (VEGF), the induction of neovascularization of these factors in the mouse cornea was studied. VEGF165 is sufficiently potent to stimulate new capillary growth from the limbal vessels. PIGF129/VEGF165 heterodimers also induce corneal neovascularization with a maximal vessel length similar to VEGF165, but with a marked decrease of vessel density. In contrast, PIGF129 has little or no effect in this in vivo angiogenesis assay. The expression of VEGF mRNA and protein is drastically up-regulated by hypoxia in choriocarcinoma cells, whereas expression of PIGF is not affected by the low concentration of oxygen. Up-regulation of VEGF production results in increased formation of PIGF/VEGF heterodimers in these tumor cells. Thus, hypoxia indirectly up-regulates expression levels of PIGF/VEGF heterodimers and modulates VEGF activity when these factors are co-expressed.

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  • Version 1 (December 1, 1996): No description

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