ArticleScientific reports2017
Gene Transfer of Prolyl Hydroxylase Domain 2 Inhibits Hypoxia-inducible Angiogenesis in a Model of Choroidal Neovascularization.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 20 citations in OpenAlex.
- VEGF in Tears as a Biomarker for Exudative Age-Related Macular Degeneration: Molecular Dynamics in a Mouse Model and Human Samples.International journal of molecular sciences · 2025Article
- A simplified protocol to induce hypoxia in a standard incubator: A focus on retinal cells.Experimental eye research · 2023Article
- Insulin-like Growth Factor-1 Prevents Hypoxia/Reoxygenation-Induced White Matter Injury in Sickle Cell Mice.Biomedicines · 2023Article
- The progress of assessment methods and treatments of neovascular glaucoma secondary to central retinal vein occlusion.Frontiers in medicine · 2023Review
- Rice Bran and Vitamin B6 Suppress Pathological Neovascularization in a Murine Model of Age-Related Macular Degeneration as Novel HIF Inhibitors.International journal of molecular sciences · 2020Article
- Gaining insight on mitigation of rubeosis iridis by UPARANT in a mouse model associated with proliferative retinopathy.Journal of molecular medicine (Berlin, Germany) · 2020Article
- Vitamin C decreases VEGF expression levels via hypoxia‑inducible factor‑1α dependent and independent pathways in lens epithelial cells.Molecular medicine reports · 2020Article
- The role of hypoxia-inducible factors in neovascular age-related macular degeneration: a gene therapy perspective.Cellular and molecular life sciences : CMLS · 2020Review
- UPARANT is an effective antiangiogenic agent in a mouse model of rubeosis iridis.Journal of molecular medicine (Berlin, Germany) · 2019Article
- Intussusceptive Vascular Remodeling Precedes Pathological Neovascularization.Arteriosclerosis, thrombosis, and vascular biology · 2019Article
- 1q42.12q42.2 Deletion in a Child with Midline Defects and Hypoplasia of the Corpus Callosum.Molecular syndromology · 2019Article
- The Different Facades of Retinal and Choroidal Endothelial Cells in Response to Hypoxia.International journal of molecular sciences · 2018Review
- Puncture-Induced Iris Neovascularization as a Mouse Model of Rubeosis Iridis.Journal of visualized experiments : JoVE · 2018Article
- Prolyl hydroxylase domain 3 influences the radiotherapy efficacy of pancreatic cancer cells by targeting hypoxia-inducible factor-1α.OncoTargets and therapy · 2018Article
- Article
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7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular responses to hypoxia are mediated by the hypoxia-inducible factors (HIF). In normoxia, HIF-α proteins are regulated by a family of dioxygenases, through prolyl and asparagyl hydroxylation, culminating in proteasomal degradation and transcriptional inactivation. In hypoxia, the dioxygenases become inactive and allow formation of HIF transcription factor, responsible for upregulation of hypoxia genes. In ocular neoangiogenic diseases, such as neovascular age-related macular degeneration (nAMD), hypoxia seems pivotal. Here, we investigate the effects of HIF regulatory proteins on the hypoxia pathway in retinal pigment epithelium (RPE) cells, critically involved in nAMD pathogenesis. Our data indicates that, in ARPE-19 cells, prolyl hydroxylase domain (PHD)2 is the most potent negative-regulator of the HIF pathway. The negative effects of PHD2 on the hypoxia pathway were associated with decreased HIF-1α protein levels, and concomitant decrease in angiogenic factors. ARPE-19 cells stably expressing PHD2 impaired angiogenesis in vitro by wound healing, tubulogenesis, and sprouting assays, as well as in vivo by iris-induced angiogenesis. Gene transfer of PHD2 in vivo resulted in mitigation of HIF-mediated angiogenesis in a mouse model of nAMD. These results may have implications for the clinical treatment of nAMD patients, particularly regarding the use of gene therapy to negatively regulate neoangiogenesis.
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