A specific phosphorylation regulates the protective role of aA-crystallin in
diabetes.
Authors Ruebsam A, Dulle JE, Myers AM, Sakrikar D, Green KM, Khan NW, Schey K, Fort PE
Submitted By Patrice Fort on 3/27/2018
Status Published
Journal JCI insight
Year 2018
Date Published 2/1/2018
Volume : Pages 3 : Not Specified
PubMed Reference 29467334
Abstract 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 a-crystallins could be involved in the
pathophysiology of diabetic retinopathy; however, the role and regulation of
a-crystallins remained unknown. In the present study, we demonstrated the
neuroprotective role of aA-crystallin during diabetes and its regulation by its
phosphorylation on residue 148. We further characterized the dual role of
aA-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 aA-crystallin as a treatment option to promote neuron
survival in diabetic retinopathy and neurodegenerative diseases in general.

Complications