SARM1 Promotes Photoreceptor Degeneration in an Oxidative Stress Model of Retinal Degeneration
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2022Access:
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Gibbons, L. and Ozaki, E. and Greene, C. and Trappe, A. and Carty, M. and Coppinger, J.A. and Bowie, A.G. and Campbell, M. and Doyle, S.L., SARM1 Promotes Photoreceptor Degeneration in an Oxidative Stress Model of Retinal Degeneration, Frontiers in Neuroscience, 16, 852114, 2022Download Item:
Abstract:
SARM1 (sterile alpha and armadillo motif-containing protein) is a highly conserved
Toll/IL-1 Receptor (TIR) adaptor with important roles in mediating immune responses.
Studies in the brain have shown that SARM1 plays a role in induction of neuronal
axon degeneration in response to a variety of injuries. We recently demonstrated
that SARM1 is pro-degenerative in a genetic model of inherited retinopathy. This
current study aimed to characterise the effect of SARM1 deletion in an alternative
model of retinal degeneration (RD) in which the retinal pigment epithelium (RPE)
fragments following administration of oxidising agent, sodium iodate (NaIO3), leading
to subsequent photoreceptor cell death. Following administration of NaIO3, we
observed no apparent difference in rate of loss of RPE integrity in SARM1 deficient
mice compared to WT counterparts. However, despite no differences in RPE
degeneration, photoreceptor cell number and retinal thickness were increased in
Sarm1−/− mice compared to WT counterparts. This apparent protection of the
photoreceptors in SARM1 deficient mice is supported by an observed decrease in
pro-apoptotic caspase-3 in the photoreceptor layer of Sarm1−/− mice compared
to WT. Together these data indicate a pro-degenerative role for SARM1 in the
photoreceptors, but not in the RPE, in an oxidative stress induced model of retinal
degeneration consistent with its known degenerative role in neurons in a range of
neurodegenerative settings.
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Frontiers in Neuroscience16
852114
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SARM1 (sterile alpha and armadillo motif-containing protein), inherited retinopathy, neuronal axon degenerationDOI:
http://dx.doi.org/10.3389/fnins.2022.852114Metadata
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