NDLI: Targeting Caspase-12 to Preserve Vision in Mice With Inherited Retinal Degeneration.

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Targeting Caspase-12 to Preserve Vision in Mice With Inherited Retinal Degeneration.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Bhootada, Yogesh Gully, Clark Gorbatyuk, Marina Choudhury, Shreyasi
Description	Country affiliation: United States Author Affiliation: Bhootada Y ( Department of Vision Sciences University of Alabama at Birmingham, Birmingham, Alabama, United States.); Choudhury S ( Department of Cell Biology and Anatomy, University of North Texas Health Science Center, North Texas Eye Research Institute, Fort Worth, Texas, United States.); Gully C ( Department of Vision Sciences University of Alabama at Birmingham, Birmingham, Alabama, United States.); Gorbatyuk M ( Department of Vision Sciences University of Alabama at Birmingham, Birmingham, Alabama, United States.)
Abstract	PURPOSE: The unfolded protein response is known to contribute to the inherited retinal pathology observed in T17M rhodopsin (T17M) mice. Recently it has been demonstrated that the endoplasmic reticulum stress-associated caspase-12 is activated during progression of retinal degeneration in different animal models. Therefore, we wanted to explore the role of caspase-12 in the mechanism of retinopathy in T17M mice and determine if inhibiting apoptosis in this way is a viable approach for halting retinal degeneration. METHODS: One, two-, and three-month-old C57BL6/J, caspase-12-/-, T17M, and T17M caspase-12-/- mice were analyzed by scotopic ERG, spectral-domain optical coherence tomography (SD-OCT), histology, quantitative (q)RT-PCR, and Western blot of retinal RNA and protein extracts. Calpain and caspase-3/7 activity assays were measured in postnatal (P) day 30 retinal extracts. RESULTS: Caspase-12 ablation significantly prevented a decline in the a- and b-wave ERG amplitudes in T17M mice during three months, increasing the amplitudes from 232% to 212% and from 160% to 138%, respectively, as compared to T17M retinas. The SD-OCT results and photoreceptor row counts demonstrated preservation of retinal structural integrity and postponed photoreceptor cell death. The delay in photoreceptor cell death was due to significant decreases in the activity of caspase-3/7 and calpain, which correlated with an increase in calpastatin expression. CONCLUSIONS: We validated caspase-12 as a therapeutic target, ablation of which significantly protects T17M photoreceptors from deterioration. Although the inhibition of apoptotic activity alone was not sufficient to rescue T17M photoreceptors, in combination with other nonapoptotic targets, caspase-12 could be used to treat inherited retinopathy.
ISSN	01460404
e-ISSN	15525783
DOI	10.1167/iovs.15-16924
Journal	Investigative Opthalmology & Visual Science
Issue Number	8
Volume Number	56
Language	English
Publisher	Association for Research in Vision and Ophthalmology
Publisher Date	2015-07-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Caspase 12 Genetics Gene Expression Regulation Retina Pathology Retinal Degeneration Animals Apoptosis Blotting, Western Biosynthesis Disease Models, Animal Electroretinography Mice Mice, Inbred C57bl Real-time Polymerase Chain Reaction Metabolism Diagnosis Tomography, Optical Coherence Research Support, N.i.h., Extramural Discipline Ophthalmology
Content Type	Text
Resource Type	Article
Subject	Ophthalmology Sensory Systems Cellular and Molecular Neuroscience

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