In addition, the upregulation of the MMP activity inhibitor, PAI-1, by all three doses of TGF-β1 as early as 6 hours post treatment is consistent with prior reports implicating PAI-1 modulation of MMP-2 activity, rather than MMP-2 transcriptional downregulation, in TGF-β1 mediated renal fibrosis [47] and provides support to our hypothesis that TGF-β1 causes increased ECM production and decreased ECM turnover, leading to the accumulation and persistence of adhesions. This evidence concerns the gene TGFB1 and renal fibrosis.