Transforming growth factor (TGF)-β is elevated in hyperuricemic individuals and mediates urate-induced hyperinflammatory phenotype in human mononuclear cells
Authors' conclusion
TGF-β is elevated in individuals with hyperuricemia and correlated to serum urate concentrations. In addition, the urate-induced pro-inflammatory phenotype in human monocytes is mediated by TGF-β signalling.
Study context
- Population
- Individuals with normouricemia, hyperuricemia and gout; Peripheral blood mononuclear cells (PBMCs) of healthy volunteers for in vitro experiments
- Comparison
- Normouricemia vs hyperuricemia vs gout; urate-exposed PBMCs with and without TGF-β blockade
- Outcome
- TGF-β levels and urate-induced inflammation
Methodological detailsin vitro validation, inhibitors of TGF-β signalling
- In vitro validation
- Inhibitors of TGF-β signalling
Main finding
As reported in the abstract
- TGF-β mRNA elevated in gout patients vs healthy controls
- Serum TGF-β-LAP significantly higher in hyperuricemia vs controls
- TGF-β correlated positively to serum urate in both cases
- In vitro, urate did not directly induce TGF-β but enhanced SMAD2 phosphorylation
- Urate-induced pro-inflammatory monocyte phenotype partly reversed by blocking TGF-β
Original publication
TGF-β is elevated in hyperuricemic individuals and mediates urate-induced hyperinflammatory phenotype in human mononuclear cells. Arthritis Res Ther. Published 27 February 2023. doi:10.
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