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Updated: Apr 30, 2026
Monitoring Dynamic Growth of Retinal Vessels in Oxygen-Induced Retinopathy Mouse Model
Published on: April 2, 2021
Fatty acid binding protein 4 deficiency protects against oxygen-induced retinopathy in mice
Magali Saint-Geniez1, Elisa Ghelfi2, Xiaoliang Liang2
1Schepens Eye Research Institute, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, United States of America.
Insights
Fatty acid binding protein 4 (FABP4) deficiency reduces pathological blood vessel growth in the eye, offering a potential target for treating retinopathy of prematurity.
Area of Science:
- Ophthalmology
- Vascular Biology
- Molecular Medicine
Background:
- Retinopathy of prematurity (ROP) is a major cause of childhood blindness.
- Pathological neovascularization in ROP is driven by vascular endothelial growth factor-A (VEGF).
- Fatty acid binding protein 4 (FABP4) is induced by VEGF and promotes angiogenesis.
Purpose of the Study:
- To investigate the role of FABP4 in retinal angiogenesis.
- To determine if FABP4 deficiency ameliorates pathological retinal vascularization in a mouse model of oxygen-induced retinopathy (OIR).
Main Methods:
- Utilized a well-characterized mouse model of oxygen-induced retinopathy (OIR).
- Analyzed FABP4 expression in retinal tissues.
- Assessed neovascularization, physiological revascularization, endothelial cell proliferation, apoptosis, and macrophage/microglia recruitment in wild-type and FABP4-/- mice.
Main Results:
- FABP4 was upregulated in neovascular tufts in OIR and localized to macrophages/microglia and hyaloid vasculature.
- FABP4-/- mice showed significantly reduced neovascularization and improved physiological revascularization.
- FABP4 deficiency led to decreased endothelial cell proliferation and reduced expression of pro-angiogenic genes.
Conclusions:
- FABP4 plays a significant role in pathological retinal angiogenesis.
- FABP4 deficiency ameliorates OIR by reducing neovascularization and improving revascularization.
- FABP4 is a potential therapeutic target for proliferative retinopathies.
Abstract:
Retinopathy of prematurity (ROP) is a leading cause of blindness in children worldwide due to increasing survival rates of premature infants. Initial suppression, followed by increased production of the retinal vascular endothelial growth factor-A (VEGF) expression are key events that trigger the pathological neovascularization in ROP. Fatty acid binding protein 4 (FABP4) is an intracellular lipid chaperone that is induced by VEGF in a subset of endothelial cells. FABP4 exhibits a pro-angiogenic function in cultured endothelial cells and in airway microvasculature, but whether it plays a role in modulation of retinal angiogenesis is not known. We hypothesized that FABP4 deficiency could ameliorate pathological retinal vascularization and investigated this hypothesis using a well-characterized mouse model of oxygen-induced retinopathy (OIR). We found that FABP4 was not expressed in retinal vessels, but was present in resident macrophages/microglial cells and endothelial cells of the hyaloid vasculature in the immature retina. While FABP4 expression was not required for normal development of retinal vessels, FABP4 expression was upregulated and localized to neovascular tufts in OIR. FABP4-/- mice demonstrated a significant decrease in neovessel formation as well as a significant improvement in physiological revascularization of the avascular retinal tissues. These alterations in retinal vasculature were accompanied by reduced endothelial cell proliferation, but no effect on apoptosis or macrophage/microglia recruitment. FABP4-/- OIR samples demonstrated decreased expression of genes involved in angiogenesis, such as Placental Growth Factor, and angiopoietin 2. Collectively, our findings suggest FABP4 as a potential target of pathologic retinal angiogenesis in proliferative retinopathies.
