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Placental growth factor stabilizes VEGF receptor-2 protein in retinal pigment epithelial cells by downregulating glycogen synthase kinase 3 activity
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| Title: | Placental growth factor stabilizes VEGF receptor-2 protein in retinal pigment epithelial cells by downregulating glycogen synthase kinase 3 activity |
| Authors: | Murata, Miyuki Browse this author →KAKEN DB | | Noda, Kousuke Browse this author →KAKEN DB | | Kase, Satoru Browse this author →KAKEN DB | | Hase, Keitaro Browse this author | | Wu, Di Browse this author | | Ando, Ryo Browse this author →KAKEN DB | | Ishida, Susumu Browse this author →KAKEN DB |
| Issue Date: | Sep-2022 |
| Publisher: | Elsevier |
| Journal Title: | Journal of Biological Chemistry (JBC) |
| Volume: | 298 |
| Issue: | 9 |
| Start Page: | 102378 |
| Publisher DOI: | 10.1016/j.jbc.2022.102378 |
| Abstract: | Placental growth factor (PlGF) belongs to the vascular endothelial growth factor (VEGF) family of proteins that participate in angiogenesis and vasculogenesis. Anti-VEGF therapy has become the standard treatment for ocular angiogenic disorders in ophthalmological practice. However, there is emerging evidence that anti-VEGF treatment may increase the risk of atrophy of the retinal pigment epithelium (RPE), which is important for the homeostasis of retinal tissue. Whereas the cytoprotective role of VEGF family molecules, particularly that of VEGF A (VEGFA) through its receptor VEGF receptor-2 (VEGFR-2), has been recognized, the physiological role of PlGF in the retina is still unknown. In this study, we explored the role of PlGF in the RPE using PlGF-knockdown RPE cells generated by retrovirus-based PlGF-shRNA transduction. We show that VEGFA reduced apoptosis induced by serum starvation in RPE cells, whereas the antiapoptotic effect of VEGFA was abrogated by VEGFR-2 knockdown. Furthermore, PlGF knockdown increased serum starvation-induced cell apoptosis and unexpectedly reduced the protein level of VEGFR-2 in the RPE. The antiapoptotic effect of VEGFA was also diminished in PlGF-knockdown RPE cells. In addition, we found that degradation of VEGFR-2 in RPE cells and inactivated by PlGF via AKT phosphorylation. Overall, the present data inactivation. |
| Type: | article |
| URI: | http://hdl.handle.net/2115/87345 |
| Appears in Collections: | 医学院・医学研究院 (Graduate School of Medicine / Faculty of Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)
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