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Long-term treatment with glucocorticoids (GCs) reportedly exaggerates renal fibrosis in chronic progressive inflammatory kidney disease. GCs induce the gene expression of plasminogen activator inhibitor-1 (PAI-1), a fibrosis enhancer in non-renal cells. Tumour necrosis factor-alpha (TNF-alpha) reduces the gene expression of 11beta-hydroxysteroid dehydrogenase (HSD) 2, an inactivator of GCs, and may enhance GC activity. However, the individual and collective effects of adrenal steroids, TNF-alpha and HSD2 status on PAI-1 production are unknown in human proximal renal tubular epithelial cells (HPTECs).

nephrology, dialysis, transplantation/nephrology dialysis transplantation

Dexamethasone enhances basal and TNF-α-stimulated production of PAI-1 via the glucocorticoid receptor regardless of 11β-hydroxysteroid dehydrogenase 2 status in human proximal renal tubular cells