Urate crystals induce macrophage PAF‑AH secretion which is differentially regulated by TGFβ1 and hydrocortisone

Article


Yagnik, D. and Hills, F. 2018. Urate crystals induce macrophage PAF‑AH secretion which is differentially regulated by TGFβ1 and hydrocortisone. Molecular Medicine Reports. 18 (3), pp. 3506-3512. https://doi.org/10.3892/mmr.2018.9323
TypeArticle
TitleUrate crystals induce macrophage PAF‑AH secretion which is differentially regulated by TGFβ1 and hydrocortisone
AuthorsYagnik, D. and Hills, F.
Abstract

The aim of the present study was to establish the role of platelet‑activating factor acetyl hydrolase (PAF‑AH) in the resolution phase of gout using an established in vitro mononuclear cell model. The effects of signalling pathway inhibitors on PAF‑AH secretion, as well as the effects of the common treatments hydrocortisone and colchicine, an antibody against the anti‑inflammatory cytokine transforming growth factor β1 (TGFβ1), and the transcriptional inhibitor actinomycin D, were also investigated. The effect of recombinant PAF‑AH on cytokine secretion by these cells was also determined. Human peripheral blood‑derived monocytes were isolated and differentiated into macrophages. Monocytes and macrophages were stimulated with monosodium monohydrate urate (MSU) crystals or lipopolysaccharide in the presence or absence of AEG3482 [a c‑Jun N‑terminal kinase (JNK) inhibitor], MG132 (a proteasome inhibitor), hydrocortisone or colchicine. Cultures were then analysed for PAF‑AH secretion using ELISA. A 6‑fold upregulation of PAF‑AH secretion was observed following macrophage exposure to MSU crystals for 24 h (29.3±6 vs. 5.4±0.3 ng/ml unstimulated; P<0.05). Following 72 h, PAF‑AH levels decreased significantly (11.1±1.8; P<0.01). Secretion was further enhanced following pre‑treatment with the JNK protein kinase inhibitor AEG3482 prior to MSU crystal stimulation (P<0.05) and was abrogated when cells were preincubated with actinomycin D or the proteasome inhibitor MG132 (50, 100 and 200 µM). The addition of recombinant PAF‑AH (2.5‑10 ng/ml) to MSU crystal‑stimulated immature monocyte cultures significantly decreased pro‑inflammatory interleukin (IL)‑1β (unstimulated 687±124 vs. stimulated 113±30 pg/ml) and IL‑6 secretion (unstimulated 590±50 vs. stimulated 182±19 pg/ml). Treatment of MSU crystal‑stimulated macrophages with hydrocortisone (2 µM) also significantly decreased PAF‑AH release (P<0.05). Neutralising anti‑TGFβ1 addition decreased PAF‑AH dose‑dependently with the highest inhibition observed at 1 µg/ml (P<0.05). The results implicated that PAF‑AH may have an anti‑inflammatory role in the resolution phase of gout.

KeywordsMolecular Medicine, Genetics, Biochemistry, Cancer Research, Oncology, Molecular Biology
Research GroupBiomarkers for Cancer group
LanguageEnglish
PublisherSpandidos Publications
JournalMolecular Medicine Reports
ISSN1791-2997
Electronic1791-3004
Publication dates
Online26 Jul 2018
Print30 Sep 2018
Publication process dates
Deposited09 Aug 2018
Accepted13 Jun 2018
Output statusPublished
Publisher's version
Copyright Statement

Reproduced with permission from Spandidos Publications
© Spandidos Publications 2018. First published in 'Molecular Medicine Reports' at: https://doi.org/10.3892/mmr.2018.9323

Digital Object Identifier (DOI)https://doi.org/10.3892/mmr.2018.9323
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