Synergy between a plasminogen cascade and MMP-9 in autoimmune disease
J. Clin. Invest. Zhi Liu, et al. 115:879 doi:10.1172/JCI23977 [Go to this article.]

Figure 2
Plasmin generation is upstream of MMP-9 activation. (A–D) actMMP-9 reconstitution restores BP in Plg^–/– mice. (A) Pathogenic anti-mBP180 IgG (R530, i.d. injection, 2.64 mg/g body weight) induced subepidermal blistering in neonatal Plg^–/– mice reconstituted with mouse Plg (5 μg/g body weight) (B) and actMMP-9 (2.5 μg/g body weight) (D) but not proMMP-9 (2.5 μg/g body weight) (C) and PBS control (A). (E–H) Plg reconstitution failed to restore BP in MMP-9^–/– mice. Pathogenic anti-mBP180 IgG (i.d. injection, 2.64 mg/g body weight) induced subepidermal blistering in neonatal MMP-9^–/– mice reconstituted with the same amount of proMMP-9 (G) and actMMP-9 (H) but not mouse Plg (F) or PBS control (E). Magnification, ×200. (I) Like +/+ mice, MMP-3^–/– mice developed extensive clinical and histological blisters (Table 1) and compatible levels of MMP activity at 12-, 24-, 48-, and 72-hour time points as determined by MMP colorimetric assay (mean ± SEM).