Open AccessMyeloid‐resident neuropilin‐1 promotes choroidal neovascularization while mitigating inflammation
Author(s) -
Andriessen Elisabeth M M A,
Binet François,
Fournier Frédérik,
Hata Masayuki,
Dejda Agnieszka,
Mawambo Gaëlle,
CrespoGarcia Sergio,
Pilon Frédérique,
Buscarlet Manuel,
Beauchemin Karine,
Bougie Véronique,
Cumberlidge Garth,
Wilson Ariel M,
Bourgault Steve,
Rezende Flavio A,
Beaulieu Normand,
Delisle JeanSébastien,
Sapieha Przemyslaw
Publication year - 2021
Publication title -
embo molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.923
H-Index - 107
eISSN - 1757-4684
pISSN - 1757-4676
DOI - 10.15252/emmm.201911754
Subject(s) - neuropilin 1 , choroidal neovascularization , macular degeneration , angiogenesis , inflammation , cancer research , neovascularization , myeloid , immunology , medicine , semaphorin , vascular endothelial growth factor , vegf receptors , receptor , ophthalmology
Age‐related macular degeneration (AMD) in its various forms is a leading cause of blindness in industrialized countries. Here, we provide evidence that ligands for neuropilin‐1 (NRP1), such as Semaphorin 3A and VEGF‐A, are elevated in the vitreous of patients with AMD at times of active choroidal neovascularization (CNV). We further demonstrate that NRP1‐expressing myeloid cells promote and maintain CNV. Expression of NRP1 on cells of myeloid lineage is critical for mitigating production of inflammatory factors such as IL6 and IL1β. Therapeutically trapping ligands of NRP1 with an NRP1‐derived trap reduces CNV. Collectively, our findings identify a role for NRP1‐expressing myeloid cells in promoting pathological angiogenesis during CNV and introduce a therapeutic approach to counter neovascular AMD.