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Intravitreal aflibercept protects photoreceptors of mice against excessive light exposure.

Abstract
Our previous studies found that an anti-placental growth factor (PlGF) antibody protected the retina in light-induced retinal damage model, a model of non-exudative age-related macular degeneration (AMD). Aflibercept is an inhibitor of vascular endothelial growth factor (VEGF) and PlGF. In present study, we revealed that the intravitreal injection of aflibercept lessens light-induced retinal damage, while anti-VEGF antibody has no effect on the light-exposed retina. Moreover, PlGF disrupted the tight junctions between the human retinal pigment epithelial cells in vitro, and aflibercept blocked the disruption. These data suggest that the aflibercept may be an effective treatment of non-exudative AMD.
AuthorsYoshiki Kuse, Kei Takahashi, Yuki Inoue, Hiroshi Izawa, Shinsuke Nakamura, Masamitsu Shimazawa, Hideaki Hara
JournalJournal of pharmacological sciences (J Pharmacol Sci) Vol. 137 Issue 4 Pg. 407-411 (Aug 2018) ISSN: 1347-8648 [Electronic] Japan
PMID30150144 (Publication Type: Journal Article)
CopyrightCopyright © 2018 The Authors. Production and hosting by Elsevier B.V. All rights reserved.
Chemical References
  • Pgf protein, mouse
  • Recombinant Fusion Proteins
  • Vascular Endothelial Growth Factor A
  • Placenta Growth Factor
  • aflibercept
  • Receptors, Vascular Endothelial Growth Factor
Topics
  • Animals
  • Cells, Cultured
  • Disease Models, Animal
  • Humans
  • Intravitreal Injections
  • Light (adverse effects)
  • Macular Degeneration (etiology, prevention & control)
  • Male
  • Mice, Inbred Strains
  • Photoreceptor Cells, Vertebrate (pathology, radiation effects)
  • Placenta Growth Factor (adverse effects, antagonists & inhibitors)
  • Receptors, Vascular Endothelial Growth Factor (administration & dosage)
  • Recombinant Fusion Proteins (administration & dosage, pharmacology)
  • Retinal Pigment Epithelium (cytology)
  • Tight Junctions (drug effects, pathology)
  • Vascular Endothelial Growth Factor A (antagonists & inhibitors)

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