Scientists Find That the Loss of a “Youth” Protein Could Drive Aging

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TOPICS:AgingEyesNational Institutes Of HealthPopularProteinRetina
By NIH/NATIONAL EYE INSTITUTE SEPTEMBER 2, 2022

TOPICS:AgingEyesNational Institutes Of HealthPopularProtein
By NIH/NATIONAL EYE INSTITUTE SEPTEMBER 2, 2022

The loss of the protein pigment epithelium-derived factor, the study discovered, is a driver of ageing-related changes in the retina.

Mice without a protective protein in their eyes have symptoms resembling age-related macular degeneration.
According to a recent National Eye Institute (NEI) study in mice, loss of the protein pigment epithelium-derived factor (PDF), which protects retinal support cells, may promote age-related changes in the retina.

Age-related retinal diseases, such as age-related macular degeneration (AMD), can cause blindness since the retina is the light-sensitive tissue at the back of the eye. The new information could help develop medicines to stop AMD and other aging conditions of the retina. The research was published in the International Journal of Molecular Sciences. NEI is part of the National Institutes of Health.
“People have called PDF the ‘youth’ protein because it is abundant in young retinas, but it declines during ageing,” said Patricia Becerra, PhD, chief of NEI’s Section of Protein Structure and Function and senior author of the study. “This study showed for the first time that just removing PDF leads to a host of gene changes that mimic ageing in the retina.”
The retina is made up of layers of cells that work together to recognize and interpret light signals, which the brain utilizes to produce vision. The retina’s light-sensing photoreceptors are located atop a layer of support cells called the retinal pigment epithelium (RPE). When photoreceptors detect light, the RPE nourishes them and recycles “outer segments,” which get used up and their tips shed each time photoreceptors detect light.

RPE from mice without Serpin1 accumulate more lipids than wild-type mice. Super-resolution confocal microscopy of RPE tissue from wild-type (upper) and Serpin1-null (lower) mice. Detailed images on the right are magnified regions of the RPE tissue imaged on the left (dotted square area). RPE cell boundaries are stained in red, and accumulated lipids are stained in green. Credit: Ivan Rebustini, NEI

Photoreceptor cells lose the capacity to create new segments and subsequently lose the ability to detect light if the RPE is unable to supply recycled components of older outer segment tips back to them. And without the nutrients that the RPE supplies, photoreceptors die. Senescence (ageing) or death of RPE cells in the retina causes vision loss in individuals with AMD or certain types of retinal dystrophies.
Previous research from Becerra’s team and other groups has shown that PDF shields retinal cells, protecting against both cellular damage and abnormal blood vessel growth in the retina. RPE cells produce and secrete the PEDF protein. The protein then binds to its receptor, PDF-R, which is also expressed by RPE cells. Binding by PDF stimulates PEDF-R to break down lipid molecules, key components of the cell membranes that enclose photoreceptor outer segments and other cellular compartments.
This breakdown step is a key part of the outer segment recycling process. And while researchers have known that PDF levels drop in the retina during the ageing process, it was not clear whether this loss of PEDF was causing, or merely correlated with, age-related changes in the retina.
To examine the retinal role of PDF, Becerra and colleagues studied a mouse model that lacks the PEDF gene (Serpin1).
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