Fig. 4: Legumain induces extracellular matrix degradation by activating MMP-2. | Cell Death & Disease

Fig. 4: Legumain induces extracellular matrix degradation by activating MMP-2.

From: Legumain is a predictor of all-cause mortality and potential therapeutic target in acute myocardial infarction

Fig. 4

A Activity of legumain in culture media after treatment with or without recombinant legumain and different concentrations of RR-11a, n = 3. B Western blot analysis of fibronectin, collagen I, and collagen III expression in TGF-β1-treated cardiac fibroblasts lysates and culture media after treatment with recombinant legumain, with or without RR-11a. C–D Quantification of collagen I, and collagen III in cell lysates (C) and supernatant (D) in (A), n = 4. E–F Gelatine zymogram for investigating MMP-2 activity in the supernatant of TGF-β1-treated cardiac fibroblasts after treatment with recombinant legumain, with or without RR-11a, n = 3. G Western blot analysis of fibronectin, collagen I, and collagen III expression in TGF-β1-treated cardiac fibroblast lysates and supernatant after treatment with recombinant legumain, with or without an MMP-2 inhibitor. H–I Quantification of fibronectin, collagen I, and collagen III in supernatant and cell lysates in (G), n = 4. *P < 0.05 vs. salinee treatment, **P < 0.05 vs. TGF-β1 treatment, #P < 0.05 vs. TGF-β1 and recombinant legumain treatment. rLegumain: recombinant legumain, Col1a1: collagens I, Col3a1: collagens III.

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