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Article

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

1
School of Pharmacy, Faculty of Health Sciences, University of Eastern Finland, 70210 Kuopio, Finland
2
Department of Clinical Chemistry, University of Helsinki and Helsinki University Hospital, 00290 Helsinki, Finland
3
Department of Ophthalmology, Institute of Clinical Medicine, University of Eastern Finland, 70210 Kuopio, Finland
4
Department of Ophthalmology, Kuopio University Hospital, 70210 Kuopio, Finland
*
Authors to whom correspondence should be addressed.
Academic Editor: Juan Pablo de Rivero Vaccari
Cells 2021, 10(6), 1405; https://doi.org/10.3390/cells10061405
Received: 24 April 2021 / Revised: 3 June 2021 / Accepted: 4 June 2021 / Published: 6 June 2021
(This article belongs to the Special Issue Inflammaging: The Immunology of Aging)
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)-1β 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-1β and IL-18 as well as NLRP3, caspase-1, and poly (ADP-ribose) polymerase (PARP). Hydroquinone did not change IL-1β release but significantly increased the secretion of IL-18. Cytoplasmic NLRP3 levels increased after the hydroquinone treatment of IL-1α-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. View Full-Text
Keywords: hydroquinone; oxidative stress; IL-1β; IL-18; NLRP3; RPE cell; PARP; DNA damage; NAC; APDC hydroquinone; oxidative stress; IL-1β; IL-18; NLRP3; RPE cell; PARP; DNA damage; NAC; APDC
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MDPI and ACS Style

Bhattarai, N.; Korhonen, E.; Mysore, Y.; Kaarniranta, K.; Kauppinen, A. Hydroquinone Induces NLRP3-Independent IL-18 Release from ARPE-19 Cells. Cells 2021, 10, 1405. https://doi.org/10.3390/cells10061405

AMA Style

Bhattarai N, Korhonen E, Mysore Y, Kaarniranta K, Kauppinen A. Hydroquinone Induces NLRP3-Independent IL-18 Release from ARPE-19 Cells. Cells. 2021; 10(6):1405. https://doi.org/10.3390/cells10061405

Chicago/Turabian Style

Bhattarai, Niina, Eveliina Korhonen, Yashavanthi Mysore, Kai Kaarniranta, and Anu Kauppinen. 2021. "Hydroquinone Induces NLRP3-Independent IL-18 Release from ARPE-19 Cells" Cells 10, no. 6: 1405. https://doi.org/10.3390/cells10061405

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