ReferenceID 5459
Hydroquinone Induces NLRP3-Independent IL-18 Release from ARPE-19 Cells
Cells
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 th
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Record Fields
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- Reference Id
- 5459
- Evidence Id
- 22049
- Core Evidence Id
- 22049
- Source Reference Id
- 4171
- Herb2 Reference Id
- HBREF004968
- Subject Paper Key
- HBIN029685_34204067
- Pubmed Id
- 34204067
- Doi
- 10.3390/cells10061405
- Paper Title
- Hydroquinone Induces NLRP3-Independent IL-18 Release from ARPE-19 Cells
- Paper 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)-1beta 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-1beta and IL-18 as well as NLRP3, caspase-1, and poly (ADP-ribose) polymerase (PARP). Hydroquinone did not change IL-1beta release but significantly increased the secretion of IL-18. Cytoplasmic NLRP3 levels increased after the hydroquinone treatment of IL-1alpha-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.
- Journal
- Cells
- Publish Year
- 2021
- Experiment Subject
- human; arpe-19 cells; il-1alpha-primed rpe cells; nonprimed cells
- Experiment Type
- Cell Experiment
- Phenotype Related
- Age-related Macular Degeneration; Impaired Vision; Retinal Disease
- Paper Title Cn
- Paper Title En
- Hydroquinone Induces NLRP3-Independent IL-18 Release from ARPE-19 Cells
- Bilingual Status
- semi_complete