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Endomucin is necessary for pathologic retinal neovascularization in vivo
Author(s) -
D'Amore Patricia A.,
ParkWindhol Cindy A.,
SaintGeniez Magali
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.lb506
Subject(s) - choroidal neovascularization , neovascularization , retinopathy of prematurity , in vivo , retinal , medicine , macular degeneration , ophthalmology , hyperoxia , retinopathy , retina , pathology , cancer research , angiogenesis , biology , endocrinology , lung , gestational age , neuroscience , pregnancy , genetics , microbiology and biotechnology , diabetes mellitus
Many ocular pathologies, including wet age‐related macular degeneration (AMD) and the retinopathy of prematurity, are characterized by abnormal neovascularization. Endomucin‐1 (EMCN), is an endothelial cell‐specific, sialic‐rich glycoprotein. We have shown that EMCN is necessary for VEGF‐mediated proliferation, migration and tube formation by human retinal endothelial cells in vitro and for normal retinal vessel development in vivo. Motivated by these finding, we examined the role of EMCN in the formation of pathological vessels using murine oxygen‐induced retinopathy (OIR) and the laser‐induced choroidal neovascularization (CNV) models. Intravitreal delivery of siEMCN to P12 mice following exposure to hyperoxia led to a significant reduction in avascular area (14.2±2.6% vs 22.6±4.7%, P<0.05) and neovascularization (2.6± 0.3% vs 3.5% ± 0.5%, P<0.05) in mice with EMCN knockdown at P17 compared to siCtrl mice. In the laser‐induced model of CNV, comparison of fluorescein angiograms at day 14 indicated that the CNV lesions in siEMCN‐treated mice were smaller and significantly less leaky than in mice (32.2±1.4% vs. 40.6±4.1%, P<0.05). Our data indicate EMCN reduction/neutralization may be a potential therapy for treating pathologic ocular neovascularization. Support or Funding Information This work was supported by EY5318 and EY26539 (PD'A), a Knight's Templar fellowship (CPW) and P30EY003790.