Inhibition of Placenta Growth Factor Reduces Subretinal Mononuclear Phagocyte Accumulation in Choroidal Neovascularization
Author(s) -
Sergio CrespoGarcia,
Caitlin Corkhill,
Christophe Roubeix,
AnjaMaria Davids,
Norbert Kociok,
Olaf Strauß,
Antonia M. Joussen,
Nadine Reichhart
Publication year - 2017
Publication title -
investigative ophthalmology and visual science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.935
H-Index - 218
eISSN - 1552-5783
pISSN - 0146-0404
DOI - 10.1167/iovs.16-21283
Subject(s) - choroidal neovascularization , aflibercept , placental growth factor , vascular endothelial growth factor , medicine , vascular endothelial growth factor a , neovascularization , macrophage polarization , growth factor , downregulation and upregulation , angiogenesis , cancer research , mononuclear phagocyte system , immune system , kinase insert domain receptor , immunology , proinflammatory cytokine , macrophage , bevacizumab , macular degeneration , biology , ophthalmology , receptor , inflammation , vegf receptors , in vitro , biochemistry , chemotherapy , gene
The cellular immune response driven by mononuclear phagocytes (MPs) is crucial for choroidal neovascularization (CNV) progression. Case reports show that a switch from pure anti-vascular endothelial growth factor-A (VEGF-A) intravitreal treatment to aflibercept, a drug with combined anti-VEGF-A and anti-placenta growth factor (PlGF) activity, can be beneficial for patients who do not respond to anti-VEGF-A alone. Since MPs harbor VEGFR1, we hypothesize that the interplay of P1GF/vascular endothelial growth factor receptor 1 (VEGFR1) in immune cells plays a pivotal role for CNV.
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