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Oxidative stress activates NLRP3 inflammasomes in ARPE‐19 cells
Author(s) -
LAAKSO N,
KINNUNEN K,
SALMINEN A,
KAARNIRANTA K,
KAUPPINEN A
Publication year - 2012
Publication title -
acta ophthalmologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.534
H-Index - 87
eISSN - 1755-3768
pISSN - 1755-375X
DOI - 10.1111/j.1755-3768.2012.f080.x
Subject(s) - inflammasome , oxidative stress , inflammation , reactive oxygen species , microbiology and biotechnology , pathogenesis , chemistry , macular degeneration , signal transduction , cytokine , biology , immunology , biochemistry , medicine , ophthalmology
Purpose Oxidative stress, which refers to cellular damage caused by reactive oxygen species (ROS), contributes to many age‐related diseases, including age‐related macular degeneration (AMD). Retinal pigment epithelial (RPE) cells must endure a high level of oxidative stress because of their high oxygen consumption, high levels of polyunsaturated lipids, and the long periods of exposure to light. Inflammation plays a major role in the pathogenesis of age‐related macular degeneration (AMD). Oxidative stress is known to activate inflammasomes, intracellular protein complexes which assemble to process the precursors of interleukin (IL)‐1beta and IL‐18 to mature and secreted cytokines by caspase‐1. In the present study, we have studied the presence of inflammasome platforms in ARPE‐19 cells. Methods After the cell exposures, ELISA and qPCR methods were used to examine the inflammasomal activity. Results In order to activate TLR pathway and NF‐kappaB signaling for inducing the production of the IL‐1beta and IL‐18 precursors, the cells were stimulated with LPS. Thereafter, 4‐hydroxynonenal (HNE) was used to provide the second signal needed for the inflammasome activation. Using the qPCR method, we showed the inflammasome receptor component to be the NACHT, LRR and PYD domains‐containing protein 3 (NLRP3). Conclusion Our data indicate that oxidative stress is able to activate NLRP3 inflammasomes in human ARPE‐19 cells.