| First Author | Pennock S | Year | 2012 |
| Journal | Mol Cell Biol | Volume | 32 |
| Issue | 10 | Pages | 1955-66 |
| PubMed ID | 22431518 | Mgi Jnum | J:185737 |
| Mgi Id | MGI:5429800 | Doi | 10.1128/MCB.06668-11 |
| Citation | Pennock S, et al. (2012) Vascular endothelial growth factor A competitively inhibits platelet-derived growth factor (PDGF)-dependent activation of PDGF receptor and subsequent signaling events and cellular responses. Mol Cell Biol 32(10):1955-66 |
| abstractText | Certain platelet-derived growth factor (PDGF) isoforms are associated with proliferative vitreoretinopathy (PVR), a sight-threatening complication that develops in a subset of patients recovering from retinal reattachment surgery. Although these PDGF isoforms are abundant in the vitreous of patients and experimental animals with PVR, they make only a minor contribution to activating PDGF receptor alpha (PDGFRalpha) and driving experimental PVR. Rather, growth factors outside of the PDGF family are the primary (and indirect) agonists of PDGFRalpha. These observations beg the question of why vitreal PDGFs fail to activate PDGFRalpha. We report here that vitreous contains an inhibitor of PDGF-dependent activation of PDGFRalpha and that a major portion of this inhibitory activity is due to vascular endothelial cell growth factor A (VEGF-A). Furthermore, recombinant VEGF-A competitively blocks PDGF-dependent binding and activation of PDGFR, signaling events, and cellular responses. These findings unveil a previously unappreciated relationship between distant members of the PDGF/VEGF family that may contribute to pathogenesis of a blinding eye disease. |
