['The plasminogen-plasmin system has potential beneficial or deleterious effects in the context of renal fibrosis. Recent studies have implicated plasminogen activators or their inhibitors in this process.', 'The development of renal interstitial fibrosis was studied in mice genetically deficient in plasminogen (plg-/- mice) and littermate controls (plg+/+ mice) by inducing unilateral ureteric obstruction (UUO) by ligating the left ureter.', 'Collagen accumulation in the kidney was decreased in plg-/- mice at 21 days compared with plg+/+ mice by hydroxyproline assay (plg+/+ 19.0 +/- 1.2 microg collagen/mg tissue, plg-/- 15.6 +/- 0.5 microg collagen/mg tissue, P= 0.04). Macrophage accumulation in plg-/- mice was reduced at 21 days, consistent with a role for plasmin in macrophage recruitment in this model. Myofibroblast accumulation, assessed by the expression of alpha-smooth muscle actin (alpha-SMA), was similar in both groups at both time points. Endogenous plasmin played a role in the activation of transforming growth factor-beta (TGF-beta), as plg-/- mice had lower ratios of betaig-h3:TGF-beta1 mRNA than plg+/+ mice. Matrix metalloproteinase (MMP)-9 activity was unchanged in the absence of plasmin, but MMP-2 activity was decreased.'] Is plasmin protective in experimental renal interstitial fibrosis?