Prevention of peritoneal adhesions: A promising role for gene therapy

Figure 1 The role of trauma, hypoxia, and inflammation in modulating molecular crosstalk in adhesion formation. tPA: Tissue plasminogen activator; PAI-1: Plasminogen activator inhibitors 1; MMP: Matrix metalloproteinase; TIMP: Tissue inhibitors of MMP; TGF-β1: Transforming growth factor-β; TNF-α: Tumor necrosis factor-α; IL: Interleukin; HIF-1α: Hypoxia inducible factor-1α; VEGF: Vascular endothelial growth factor; CTGF: Connective tissue growth factor.

Figure 2 Correlation analysis was performed using two-tailed Spearmen rank correlation test between tPA with respect to PAI-1 (line A, marker 〇), TIMP-1 (line B, marker ◇), TGF-β1 (line C, marker ▽) or adhesion score (line D, marker □). Values of tPA, PAI-1, TIMP-1, and TGF-β1 concentration in adhesion tissues were logarithmically transformed to obtain a normal distribution before statistical analysis. There was significant negative correlations (P < 0.01) between human tPA and either of PAI-1 (Spearman rank correlation coefficient, r = -0.89), TIMP-1 (r = -0.73), TGF-β1 (r = -0.87), or adhesion score (r = -0.87). tPA: Tissue plasminogen activator; PAI-1: Plasminogen activator inhibitors 1; TIMP: Tissue inhibitors of MMP; TGF-β1: Transforming growth factor-β.

Figure 3 Skeleton of a conventional plasmid. Ori: Origin of replication.