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Aging and age-related diseases affect eye health in different ways. Chris Zielecki/Getty Images

  • The “youth” protein, pigment epithelium-derived factor (PEDF), protects cells in the eye’s retina from oxidative stress, a new animal study shows.
  • Researchers with the National Eye Institute (NEI) found that declines in PEDF levels may contribute to aging-related diseases of the retina.
  • Experts hope these findings will lead to developing new therapies that can reverse or counter the effects of PEDF loss.

The retina is composed of tissues in the back associated with the eye that process light signals and send them to the brain. Retinal color epithelium (RPE) cells make up part of this important structure with regard to vision.

A recent animal study by the Country wide Eye Company , part associated with the National Institutes of Health , suggests that will the loss of a certain protein could cause RPE cells to stop nourishing and recycling photoreceptor tissues.

The resulting senescence or even deterioration of RPE tissue may trigger the onset of diseases like age-related macular degeneration (AMD) plus retinal dystrophies . These conditions are known to cause progressive vision loss.

The team led by Dr. Patricia Becerra , senior investigator at the NEI’s Section associated with Protein Structure and Function, discovered that the particular pigment epithelium-derived factor (PEDF) plays an anti-aging function for RPE cells. Their findings could offer the potential for finding new ways to treat or prevent aging-associated retinal illnesses.

This study was published in the International Journal of Molecular Sciences .

The RPE produces and secretes PEDF via the Serpinf1 gene. PEDF is called the particular “youth” proteins due to its abundance in young retinas.

RPE production plus PEDF secretion decline during senescence and aging in the eyes, skin, lungs, and other tissues.

Earlier research suggests that PEDF can protect photoreceptor cells through damage plus inhibit the growth associated with abnormal blood vessels in the particular eye.

However, Dr . Becerra stated: “We always wondered if reduction of PEDF was driven by aging or was driving aging. ”

To find the answer, Doctor Becerra and her colleagues used the mouse model bioengineered without the PEDF gene Serpinf1 .

Looking into the cellular structure of the models’ retinas, the researchers discovered remarkable differences from the particular control samples of wild-type mice.

The RPE cell nuclei were enlarged, which could indicate differences in how the cells’ DNA was arranged. These cellular material had also activated four genes associated with mobile senescence plus aging.

Dr. Ivan Rebustini , a staff scientist in Dr . Becerra’s lab and the study’s lead author, remarked: “One of the particular most striking things has been this reduction in the PEDF receptor on the surface of the RPE cells within the mouse lacking the particular PEDF protein. It seems there’s some sort of feedback-loop involving PEDF […]”

These changes led the team in order to conclude that PEDF decline prompts the aging of retinal cells.

This research may uncover ways to help reduce age-related vision problems, but it does come with a few limitations.

What’s causing PEDF loss?

Although the research proposes that will PEDF might drive aging, its results do not answer what’s causing PEDF loss.

In an interview with Healthcare News Today, Dr. Becerra explained: “Besides PEDF, there are other proteins that are dysregulated in various epithelial tissues—including the RPE—during aging. Besides changes within the expression and production of aging-related proteins, telomere shortening has been associated with aging, and is observed in epithelial cells with high turnover, like the skin. ”

“Telomeres are a structure at the end of a chromosome that maintains the integrity of our genes and are a critical factor regarding age-related diseases. Their shortening can impact the manifestation of genes during ageing; the PEDF gene, Serpinf1, is one associated with them, ” she continued.

“However, the extent to which this is driving PEDF loss in the eye is unknown, ” she added.

MNT furthermore discussed this study along with Doctor Howard R. Krauss , surgical neuro-ophthalmologist of Pacific Neuroscience Institute in Providence Saint John’s Wellness Center inside Santa Monica, CA, who was not really involved in this study.

Dr . Krauss shared that while “we understand the particular vital importance of this particular protein plus […] that will its availability declines with age and/or degenerative disease, [w]e do not know what causes the loss. ”

He agreed that PEDF depletion is just one of many factors behind RPE aging. This individual noted that will identifying more factors may be necessary for reducing or even reversing age-related damage.

Mouse-to-human trial challenges

The present work analyzed mouse models, which would be difficult to translate to human trials, Doctor Krauss cautioned.

For instance, Dr . Becerra noted that “the lack of a macula within the mouse’s retina means the parallels in order to conditions like age-related macular degeneration are not as clear as they might be within a species with that will structure. ”

According to Doctor Krauss: “[T]here will be no assurance that what may work in this computer mouse model will ultimately be of value in humans. ”

Further, Dr. Becerra told MNT that, because samples from patients without PEDF are usually scarce, replicating the study in humans would be challenging.

The study’s applications

Nevertheless, Dr . Krauss was somewhat optimistic about the implications of this NIH analysis.

He or she hoped that the demonstration of the particular effects of PEDF loss “will now allow the use of this design to apply potential therapeutic measures to increase PEDF and/or the application of proposed restorative measures in order to counteract the damaging associated with PEDF depletion. ”

Dr. Becerra said that will she and fellow researchers will continue exploring “ways to use PEDF-derived peptides or mimics as a therapeutic for people. ”

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