Figure 7
Figure 7. Model depicting CD36-dependent antiangiogenic pathways. VEGFR2 forms a complex with CD36. When CD36 is not engaged by its ligand, TSP-1, VEGF binding to VEGFR2 induces VEGFR2 phosphorylation at Tyr1175 and promotes MVEC migration and tube formation. Engagement of CD36 by TSP-1 leads to inhibition of migration and tube formation by 2 independent processes. Recruitment of SHP-1 to the VEGFR2-CD36 complex leads to dephosphorylation of VEGFR2 (Tyr1175), thus dampening VEGF signaling, and activation of Fyn leads to apoptosis via activation of MAP kinases and caspases. Syk may participate in these pathways, although the mechanisms remain undefined.

Model depicting CD36-dependent antiangiogenic pathways. VEGFR2 forms a complex with CD36. When CD36 is not engaged by its ligand, TSP-1, VEGF binding to VEGFR2 induces VEGFR2 phosphorylation at Tyr1175 and promotes MVEC migration and tube formation. Engagement of CD36 by TSP-1 leads to inhibition of migration and tube formation by 2 independent processes. Recruitment of SHP-1 to the VEGFR2-CD36 complex leads to dephosphorylation of VEGFR2 (Tyr1175), thus dampening VEGF signaling, and activation of Fyn leads to apoptosis via activation of MAP kinases and caspases. Syk may participate in these pathways, although the mechanisms remain undefined.

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