Placental growth factor stabilizes VEGF receptor-2 protein in retinal pigment epithelial cells by downregulating glycogen synthase kinase 3 activity

Murata, Miyuki; Noda, Kousuke; Kase, Satoru; Hase, Keitaro; Wu, Di; Ando, Ryo; Ishida, Susumu

Placental growth factor stabilizes VEGF receptor-2 protein in retinal pigment epithelial cells by downregulating glycogen synthase kinase 3 activity

Murata, Miyuki; Noda, Kousuke; Kase, Satoru et al.

Journal of Biological Chemistry (JBC), 2022, 298(9), 102378

Permalink : https://hdl.handle.net/2115/87345

このアイテムのアクセス数:367件（2026-08-24 20:31 集計）

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https://doi.org/10.1016/j.jbc.2022.102378			12

論文情報

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アクセス権	open access
URI	https://hdl.handle.net/2115/87345
タイトル	Placental growth factor stabilizes VEGF receptor-2 protein in retinal pigment epithelial cells by downregulating glycogen synthase kinase 3 activity
著者	Murata, Miyuki ; Noda, Kousuke ; Kase, Satoru ; Hase, Keitaro ; Wu, Di ; Ando, Ryo ; Ishida, Susumu
e-Rad_Researcher 50423752 著者名 Murata, Miyuki
e-Rad_Researcher 90296666 著者名 Noda, Kousuke
e-Rad_Researcher 60374394 著者名 Kase, Satoru
著者名 Hase, Keitaro
著者名 Wu, Di
e-Rad_Researcher 60399847 著者名 Ando, Ryo
e-Rad_Researcher 10245558 著者名 Ishida, Susumu
言語	英語
発行日	2022-09
出版者	Elsevier
収録物名	Journal of Biological Chemistry (JBC)
巻(号)	298(9)
ページ	102378
抄録	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.
資源タイプ	学術雑誌論文
出版タイプ	Version of Record
関連情報 (isIdenticalTo)	出版社版DOI https://doi.org/10.1016/j.jbc.2022.102378