Skip to main content
. 2016 Jun 24;6:28627. doi: 10.1038/srep28627

Figure 8. A schematic illustration of PDGF-IRE1α-XBP1-miR-150 pathway in EC-SMC interaction.

Figure 8

Under ischemia, the activated ECs may secret PDGF, which in turn activates IRE1α phosphorylation, leading to XBP1 mRNA splicing to remove 26-nucleotide intron in SMCs. The spliced XBP1 stabilizes miR-150 and increases its secretion via extracellular vesicles (EVs). The miR-150-containing EVs are taken by ECs, increasing VEGF-A mRNA transcription or stability, leading to VEGF-A protein production and secretion. VEGF-A triggers the ErK and Akt phosphorylation via binding to VEGF receptor in an autocrine or paracrine manner. The activated Akt contributes to EC migration, leading to angiogenesis.