Good news! Will we soon be able to prevent age related deterioration in our eyesight? Quite possible!
"... Experiments on mice missing this protein led to fast-tracked degeneration in the retina, indicating that the protein plays an important protective role against age-related vision loss. ...
the study centers on a protein called pigment epithelium-derived factor (PEDF). This protein plays an important mediatory role in a natural recycling process in the eye. It is produced by a layer of support cells, called the retinal pigment epithelium (RPE), which sits beneath the retina's light-sensing photoreceptor cells and helps recycle and replenish them as their outer edges wear out. This ability declines as we grow older and in people with age-related macular degeneration (AMD), leading to vision loss. ..."
the study centers on a protein called pigment epithelium-derived factor (PEDF). This protein plays an important mediatory role in a natural recycling process in the eye. It is produced by a layer of support cells, called the retinal pigment epithelium (RPE), which sits beneath the retina's light-sensing photoreceptor cells and helps recycle and replenish them as their outer edges wear out. This ability declines as we grow older and in people with age-related macular degeneration (AMD), leading to vision loss. ..."
From the abstract:
"The retinal pigment epithelium (RPE) expresses the Serpinf1 gene to produce pigment epithelium-derived factor (PEDF), a retinoprotective protein that is downregulated with cell senescence, aging and retinal degenerations. We determined the expression of senescence-associated genes in the RPE of 3-month-old mice that lack the Serpinf1 gene and found that Serpinf1 deletion induced H2ax for histone H2AX protein, Cdkn1a for p21 protein, and Glb1 gene for β-galactosidase. Senescence-associated β-galactosidase activity increased in the Serpinf1 null RPE when compared with wild-type RPE. We evaluated the subcellular morphology of the RPE and found that ablation of Serpinf1 increased the volume of the nuclei and the nucleoli number of RPE cells, implying chromatin reorganization. Given that the RPE phagocytic function declines with aging, we assessed the expression of the Pnpla2 gene, which is required for the degradation of photoreceptor outer segments by the RPE. We found that both the Pnpla2 gene and its protein PEDF-R declined with the Serpinf1 gene ablation. Moreover, we determined the levels of phagocytosed rhodopsin and lipids in the RPE of the Serpinf1 null mice. The RPE of the Serpinf1 null mice accumulated rhodopsin and lipids compared to littermate controls, implying an association of PEDF deficiency with RPE phagocytosis dysfunction. Our findings establish PEDF loss as a cause of senescence-like changes in the RPE, highlighting PEDF as both a retinoprotective and a regulatory protein of aging-like changes associated with defective degradation of the photoreceptor outer segment in the RPE."
NIH study finds loss of ‘youth’ protein may drive aging in the eye Eyes of mice lacking protective protein show signs similar to age-related macular degeneration
No comments:
Post a Comment