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Hyperhomocysteinemia caused chorioretinal vasculopathy in an animal model
Author(s) -
Lee Y.J.,
Ke C.Y.,
Lin P.K.
Publication year - 2016
Publication title -
acta ophthalmologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.534
H-Index - 87
eISSN - 1755-3768
pISSN - 1755-375X
DOI - 10.1111/j.1755-3768.2016.0362
Subject(s) - hyperhomocysteinemia , medicine , macular degeneration , vascular endothelial growth factor , choroid , retina , homocysteine , retinal , pathogenesis , placental growth factor , ophthalmology , pathology , vegf receptors , biology , neuroscience
Purpose Many reports have suggested that hyperhomocysteinemia is a risk factor for atherosclerosis. Some of the reports further indicated that hyperhomocysteinemia was associated with neural degenerative diseases and even age‐related macular degeneration (AMD). However, the pathogenesis of AMD has not been elucidated clearly yet. We therefore established an animal model to mimic hyperhomocysteinemia status in vivo . Morphological changes of chorioretina, and possibly involved growth factors were investigated in this study. Methods The hyperhomocysteinemia animal model was generated by administering various doses of homocysteine via intravenous injection to Sprague‐Dawley rats. Chorioretinal images from the rat models in the different treatment groups were recorded, and fluoresceine angiographies (FAG) were done. Histological examinations of the retina and choroid were also performed. Immunofluorescent studies were used to investigate the expression levels of vascular cell markers and different types of vascular endothelial growth factors (VEGF). Results Significantly prominent choroidal vasculatures with congestion and retinal vascular disorders were observed in the chorioretinal images and FAGs of the hyperhomocysteinemic animals. The choroidal capillary plexuses were disclosed expanded and vascular endothelial cells proliferated in the histological examinations. We also found the expressions of VEGF and placental growth factor (PlGF) were both upregulated in the eyes of the animals. Conclusions Hyperhomocysteinemia caused choroidal vascular proliferation. VEGF and PlGF might mainly mediate this situation, and PlGF played a key role in that.