The researchers believe these results provide a new basic comprehension of fetal eye progression and ocular conditions caused by vascular issues.
The study, conducted by scientists from Cincinnati's Children's Hospital Medical Center and the University of California, San Francisco (UCSF), and published in the journal Nature, reveals information about retinopathy prematurity that causes blindness in babies that are born prematurely.
Co-author Richard Lang, PhD, a researcher in the Division of Pediatric Ophthalmology at Cincinnati Children's Hospital Medical Center said:
"This fundamentally changes our understanding of how the retina develops. We have identified a light-response pathway that controls the number of retinal neurons. This has downstream effects on developing vasculature in the eye and is important because several major eye diseases are vascular diseases."
Lang collaborated with David Copenhagen, PhD, a scientist in the departments of Opthalmology and Physiology at UCSF. The two used mouse models to execute their study and discovered several surprising outcomes.
Copenhagen commented, "Several stages of mouse eye development occur after birth. Because of this, we had always assumed that if light played a role in the development of the eye, it would also happen only after birth."
The researchers in the current study revealed that the activation of the newly labeled light-response pathway must occur during pregnancy in order to achieve the precisely planned program that creates a normal eye. They point out that it is crucial for the right number of photons to reach the mother's body by late term pregnancy, or for a mouse pregnancy, roughly 16 days.
Additionally, the scientists saw that photons of light trigger a protein called melanopsin inside the fetus, not the mother, to aid in the beginning of healthy blood vessel and retinal neuron development in the eye.
One function of the light-response pathway is to hold back the number of blood vessels that form in the retina. These vessels are essential to retinal neurons, which need more amounts of oxygen to development and work.
When retinopathy of prematurity happens in babies, retinal vessels progress nearly unchecked. Their continued progression causes extreme pressure on the new eye and in severe cases produces grave damage or blindness.
Impact of the light-response pathwayThe team of scientists completed several experiments using laboratory mouse models that let them look at the light-response pathway's particular purpose and parts.
Mice were raised in darkness, and in a regular day-night cycle starting at late term pregnancy to examine the comparative outcomes on vascular progression of the eye.
The scientists confirmed the purpose of the light response pathway by changing an opsin gene in mice known as Opn4 that creates melanopsin, in other words, stopping the initiation of the photo pigment.
Mice with mutated Opn4, as well as those that were raised in darkness, showed similar random expansion of hyaloid vessels and unusual retinal vascular progression. The unchecked vascular progression was powered by the protein vascular endothelial growth factor (Vegfa). When the light response pathway is functioning correctly, it adjusts Vegfa to ward off indiscriminate vascular expansion, the researchers suggest.
The melanopsin protein is there in both humans and mice during pregnancy. The authors say they will continue to examine how the light-response pathway might impact the probability of pre-term babies developing retinopathy of prematurity and its relatedness to other eye conditions.
Written by Kelly Fitzgerald