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A specific phosphorylation regulates the protective role of αA-crystallin in diabetes.

Ruebsam A, Dulle JE, Myers AM, Sakrikar D, Green KM, Khan NW, Schey K, Fort PE
JCI Insight. 2018 3 (4)

PMID: 29467334 · PMCID: PMC5916248 · DOI:10.1172/jci.insight.97919

Neurodegeneration is a central aspect of the early stages of diabetic retinopathy, the primary ocular complication associated with diabetes. While progress has been made to improve the vascular perturbations associated with diabetic retinopathy, there are still no treatment options to counteract the neuroretinal degeneration associated with diabetes. Our previous work suggested that the molecular chaperones α-crystallins could be involved in the pathophysiology of diabetic retinopathy; however, the role and regulation of α-crystallins remained unknown. In the present study, we demonstrated the neuroprotective role of αA-crystallin during diabetes and its regulation by its phosphorylation on residue 148. We further characterized the dual role of αA-crystallin in neurons and glia, its essential role for neuronal survival, and its direct dependence on phosphorylation on this residue. These findings support further evaluation of αA-crystallin as a treatment option to promote neuron survival in diabetic retinopathy and neurodegenerative diseases in general.

MeSH Terms (23)

Aged alpha-Crystallin A Chain alpha-Crystallin B Chain Animals Cell Line Crystallins Diabetes Mellitus, Experimental Diabetic Retinopathy Electroretinography Ependymoglial Cells Female Humans Male Mice Mice, Knockout Neurons Phosphorylation Rats Rats, Sprague-Dawley Recombinant Proteins Retina Streptozocin Transfection

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