Moran Eye Center publishes retinopathy of prematurity research

Salt Lake City, UT-The University of Utah’s John A. Moran Eye Center has published a research paper examining the role of erythropoietin (EPO) signaling in retinopathy of prematurity (ROP) in the American Journal of Pathology.

Common to most forms of ROP is the over activation of vascular endothelial growth factor (VEGF) signaling, which can cause disordered blood vessel growth. However, VEGF plays a vital role in the development of the retina and other organs in developing preterm infants, so Moran researchers focused this research on discovering mechanisms to regulate VEGF signaling without adversely reducing its beneficial effects.

Researchers used the rat oxygen-induced retinopathy (OIR) model, the most representative model of human ROP, to study the role of EPO signaling in ROP. EPO has been given to preterm infants to combat anemia and is being considered as a neuroprotective agent. Using the OIR model, researchers found that EPO receptors were activated even when EPO was not increased, and that increased VEGF actually resulted in the activation of both EPO and VEGF receptors, which together led to pathologic angiogenesis.

“This is an exciting development, because it opens up the potential for targeting EPO receptors in endothelial cells to regulate VEGF signaling, which is dysregulated in ROP. In addition, regulation of VEGF signaling in this way could eliminate the occurrence of ROP developing if EPO is given for neural and cognitive development,” says Mary Elizabeth Hartnett, MD, principal investigator at the Moran Eye Center’s Retinal Angiogenesis Laboratory and corresponding author to the research paper. “The availability of preterm infant eyes for research studies is limited, but previous research at Moran demonstrated that by using this OIR model, we can generate many of the same conditions that preterm infants experience who develop ROP.”