Hydroquinone Induces NLRP3-Independent IL-18 Release from ARPE-19 Cells

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http://hdl.handle.net/10138/332367

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Bhattarai , N , Korhonen , E , Mysore , Y , Kaarniranta , K & Kauppinen , A 2021 , ' Hydroquinone Induces NLRP3-Independent IL-18 Release from ARPE-19 Cells ' , Cells , vol. 10 , no. 6 , 1405 . https://doi.org/10.3390/cells10061405

Title: Hydroquinone Induces NLRP3-Independent IL-18 Release from ARPE-19 Cells
Author: Bhattarai, Niina; Korhonen, Eveliina; Mysore, Yashavanthi; Kaarniranta, Kai; Kauppinen, Anu
Contributor organization: HUSLAB
University of Helsinki
Helsinki University Hospital Area
Date: 2021-06
Language: eng
Number of pages: 14
Belongs to series: Cells
ISSN: 2073-4409
DOI: https://doi.org/10.3390/cells10061405
URI: http://hdl.handle.net/10138/332367
Abstract: Age-related macular degeneration (AMD) is a retinal disease leading to impaired vision. Cigarette smoke increases the risk for developing AMD by causing increased reactive oxygen species (ROS) production and damage in the retinal pigment epithelium (RPE). We have previously shown that the cigarette tar component hydroquinone causes oxidative stress in human RPE cells. In the present study, we investigated the propensity of hydroquinone to induce the secretion of interleukin (IL)-1 beta and IL-18. The activation of these cytokines is usually regulated by the Nucleotide-binding domain, Leucine-rich repeat, and Pyrin domain 3 (NLRP3) inflammasome. ARPE-19 cells were exposed to hydroquinone, and cell viability was monitored using the lactate dehydrogenase (LDH) and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide salt (MTT) assays. Enzyme-linked immunosorbent assays (ELISAs) were used to measure the levels of proinflammatory cytokines IL-1 beta and IL-18 as well as NLRP3, caspase-1, and poly (ADP-ribose) polymerase (PARP). Hydroquinone did not change IL-1 beta release but significantly increased the secretion of IL-18. Cytoplasmic NLRP3 levels increased after the hydroquinone treatment of IL-1 alpha-primed RPE cells, but IL-18 was equally released from primed and nonprimed cells. Hydroquinone reduced the intracellular levels of PARP, which were restored by treatment with the ROS scavenger N-acetyl-cysteine (NAC). NAC concurrently reduced the NLRP3 levels but had no effect on IL-18 release. In contrast, the NADPH oxidase inhibitor ammonium pyrrolidinedithiocarbamate (APDC) reduced the release of IL-18 but had no effect on the NLRP3 levels. Collectively, hydroquinone caused DNA damage seen as reduced intracellular PARP levels and induced NLRP3-independent IL-18 secretion in human RPE cells.
Subject: 3111 Biomedicine
1182 Biochemistry, cell and molecular biology
hydroquinone
oxidative stress
IL-1 beta
IL-18
NLRP3
RPE cell
PARP
DNA damage
NAC
APDC
PIGMENT EPITHELIUM-CELLS
NLRP3 INFLAMMASOME ACTIVATION
MACULAR DEGENERATION AMD
INDUCED DNA-DAMAGE
PROTECTIVE IMMUNITY
INDUCED APOPTOSIS
OXIDATIVE STRESS
RESPONSES
RECEPTOR
ATP
Peer reviewed: Yes
Rights: cc_by
Usage restriction: openAccess
Self-archived version: publishedVersion


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