YALE PATHOLOGY - Research Labs

Figure 3A & 3B
Hypoxia-induced endothelial BDNF mediates endothelial survival and differentiation via an autocrine loop and neural progenitor survival, proliferation and differentiation by a paracrine loop, which then induces NPC NO, which in turn supports EC survival and differentiation via a paracrine loop and NPC survival, proliferation and differentiation via an autocrine loop.

Figure 3C
Hypoxia induces EC BDNF, which in turn induces NPC, NO, via TrkB signaling, activating a PI3K/Akt pathway, inducing expression and activation of eNOS. NO signaling, in turn, stabilizing HIF-1alpha and decreases Prolyl Hydroxylase Domain 2, inducing persistent EC BDNF (and VEGF & SDF-1), which facilitate continued NO generation and NPC survival, proliferation and differentiation.