Research ArticleVASCULAR BIOLOGY

The interaction of uPAR with VEGFR2 promotes VEGF-induced angiogenesis

See allHide authors and affiliations

Science Signaling  17 Nov 2015:
Vol. 8, Issue 403, pp. ra117
DOI: 10.1126/scisignal.aaa2403

You are currently viewing the editor's summary.

View Full Text

Log in to view the full text

Log in through your institution

Log in through your institution

Helping a proangiogenic receptor

Vascular endothelial growth factor (VEGF) induces the formation of new blood vessels, a process called angiogenesis, upon binding to VEGFR2, a cell surface receptor for which internalization enhances its ability to activate downstream effectors. Herkenne et al. found that in response to VEGF, another receptor called uPAR (urokinase plasminogen activator receptor) promoted an interaction between another receptor LRP-1 (low-density lipoprotein receptor–related protein 1), and VEGFR2, which led to VEGF2 internalization, thus enhancing the signal. Mice deficient in uPAR showed reduced VEGF-induced angiogenesis. Thus, treatments that disrupt the interaction between uPAR and VEGFR2 could be used to treat conditions in which angiogenesis is not desirable, such as in solid tumors or diabetic retinopathy.

View Full Text