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Fatty Acid Binding Protein 4‐deficient Mice are Protected from Oxygen‐induced Retinal Neovascularization
Author(s) -
Saint-Geniez Magali,
Ghelfi Elisa,
D'Amore Patricia,
Hotamisligil Gökhan,
Cataltepe Sule
Publication year - 2012
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.26.1_supplement.832.9
Subject(s) - fatty acid binding protein , retinal , neovascularization , immunostaining , endocrinology , medicine , biology , angiogenesis , chemistry , biochemistry , immunohistochemistry , gene
Fatty acid binding protein 4 (FABP4) is a member of the FABP family, which consists of highly conserved proteins that function as chaperones for free fatty acids. FABP4 plays a critical role in maintenance of glucose and lipid homeostasis as well as in the regulation of inflammation. Initially, FABP4 was thought to be expressed primarily by adipocytes and macrophages. We recently determined that FABP4 is also expressed in certain endothelial cells (ECs) where it plays a pro‐angiogenic role. The goal of this study was to determine whether FABP4 plays a role in oxygen‐induced retinal neovascularization. We induced oxygen‐induced retinopathy (OIR) by exposing pups to 75% oxygen between postnatal (P) days 7 and 12. FABP4 mRNA and protein levels were significantly increased during OIR. Immunostaining revealed that FABP4 was strongly expressed in pathological neovessels but absent in normal retinal vessels. In addition, both the neovascular and avascular areas of FABP4−/− retinas were significantly reduced at P17 compared to WT. The effect of FABP4 deficiency on OIR appears independent from macrophages recruitment. The observations that FABP4‐deficient mice are significantly protected from OIR and that FABP4 expression is restricted to neovascular tufts suggests that FABP4 inhibition may be a potential therapeutic target for proliferative retinopathies. This project is funded by the NEI grant 1R21EY021873‐01.