Caspase-1-dependent inflammasomes mediate photoreceptor cell death in photo-oxidative damage-induced retinal degeneration.

Abstract:

:Activation of the inflammasome is involved in the progression of retinal degenerative diseases, in particular, in the pathogenesis of Age-Related Macular Degeneration (AMD), with NLRP3 activation the focus of many investigations. In this study, we used genetic and pharmacological approaches to explore the role of the inflammasome in a mouse model of retinal degeneration. We identify that Casp1/11-/- mice have better-preserved retinal function, reduced inflammation and increased photoreceptor survivability. While Nlrp3-/- mice display some level of preservation of retinal function compared to controls, pharmacological inhibition of NLRP3 did not protect against photoreceptor cell death. Further, Aim2-/-, Nlrc4-/-, Asc-/-, and Casp11-/- mice show no substantial retinal protection. We propose that CASP-1-associated photoreceptor cell death occurs largely independently of NLRP3 and other established inflammasome sensor proteins, or that inhibition of a single sensor is not sufficient to repress the inflammatory cascade. Therapeutic targeting of CASP-1 may offer a more promising avenue to delay the progression of retinal degenerations.

journal_name

Sci Rep

journal_title

Scientific reports

authors

Wooff Y,Fernando N,Wong JHC,Dietrich C,Aggio-Bruce R,Chu-Tan JA,Robertson AAB,Doyle SL,Man SM,Natoli R

doi

10.1038/s41598-020-58849-z

subject

Has Abstract

pub_date

2020-02-10 00:00:00

pages

2263

issue

1

issn

2045-2322

pii

10.1038/s41598-020-58849-z

journal_volume

10

pub_type

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