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A new study shows major progress toward isolating the causes of ROP.
Salt Lake City-A new study published by The University of Utah’s John A. Moran Eye Center shows major progress toward isolating the underlying causes of retinopathy of prematurity (ROP).
Researchers are closer to suppressing effects from specific cells that overproduce vascular endothelial growth factor (VEGF), but also other organs in human infants, including the brain, kidney, and lungs. Overproduction of VEGF could lead to blindness in pre-term infants.
The study, which is published in the September issue of the American Journal of Pathology, also uses rats, not mice, in a more representative study model of human ROP in pre-term infants. But it proposes modifying the rat oxygen-induced retinopathy (OIR) model using gene delivery approaches which will allow researchers to regulate the production of VEGF to combat ROP without negatively compromising other prenatal growth.
Because studying fragile human preterm infant eyes to understand ROP is unsafe, researchers typically use a mouse model of OIR to examine the production of VEGF and for the development of treatment options. Using a rat OIR model is actually more representative of human ROP, but using this model requires pharmacological manipulations that do not determine specific cells that overproduce VEGF or how VEGF causes growth of abnormal, instead of normal, blood vessels. Use of molecular methods improves the rigor of the model and also targets pathologic pathways while sparing normal pathways.
This study was funded by the National Eye Institute (grant EY015130).