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• W2011416774 abstract "Background Factors associated with postthrombotic syndrome are known clinically, but the underlying cellular processes at the vein wall are not well delineated. Prior work suggests that vein wall damage does not correlate with thrombus resolution but rather with plasminogen activator-1 (PAI-1) and matrix metalloproteinase (MMP) activity. Objective We hypothesized that PAI-1 would confer post venous thrombosis (VT) vein wall protection via a vitronectin (Vn)-dependent mechanism. Methods A stasis model of VT was used with harvest over 2 weeks, in wild-type, Vn−/−, and PAI-1–overexpressing mice (PAI-1 Tg). Results PAI-1 Tg mice had larger VT at 6 and 14 days, compared to controls, but Vn−/− mice had no alteration of VT resolution. Gene deletion of Vn resulted in an increase in, rather than the expected decrease in, circulating PAI-1 activity. While both Vn−/− and PAI-1 Tg had attenuated intimal fibrosis, PAI-1 Tg had significantly less vein wall collagen and a compensatory increase in collagen III gene expression. Both Vn−/− and PAI-1 Tg vein wall had less monocyte chemotactic factor-1 and fewer macrophages (F4/80), with significantly less MMP-2 activity and decreased TIMP-1 antigen. Ex vivo assessment of transforming growth factor β–mediated fibrotic response showed that PAI-1 Tg vein walls had increased profibrotic gene expression (collagens I and III, MMP-2, and α–smooth muscle actin) compared with controls, opposite of the in vivo response. Conclusions The absence of Vn increases circulating PAI-1, which positively modulates vein wall fibrosis in a dose-dependent manner. Translationally, PAI-1 elevation may decrease vein wall damage after deep vein thrombosis, perhaps by decreasing macrophage-mediated activities." @default.
• W2011416774 created "2016-06-24" @default.
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• W2011416774 date "2014-08-01" @default.
• W2011416774 modified "2023-10-14" @default.
• W2011416774 title "Plasminogen activator‐1 overexpression decreases experimental postthrombotic vein wall fibrosis by a non‐vitronectin‐dependent mechanism" @default.
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• W2011416774 doi "https://doi.org/10.1111/jth.12644" @default.
• W2011416774 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4127110" @default.
• W2011416774 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24943740" @default.
• W2011416774 hasPublicationYear "2014" @default.
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