Hypoxia-induced increases in HIF-1 levels can stimulate the transcription and translation of multiple Receptor Tyrosine Kinase-dependent vasotrophic factors. HIF-induced increases in FGF have been shown to stabilize HIF-1α, effectively enhancing its own synthesis. Increases in VEGF and VEGF receptors can induce endothelial cell proliferation. In addition to having angiogenic effects, VEGF can also be neuroprotective, can induce endothelial cell proliferation and vascular remodeling. VEGF can also activate PDGF receptors. Hypoxia causes an increase in VEGF, Angiopoietin 1 (Ang1), and PDGF-B levels, which activate Akt and inhibit apoptosis, particularly in neurons.