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. 2014 Mar 26;34(6):1047–1059. doi: 10.1038/jcbfm.2014.54

Figure 5.

Figure 5

Increased matrix metalloproteinase (MMP)-3, MMP-10, and MMP-12 activities in human brain microvascular endothelial cells (HBMEC) treated with Tat.B compared with cells treated with Tat.AG. HBMEC were treated with Tat.B or Tat.AG at 1 to 1,000 ng/mL for 48 hours and MMPs activity in culture supernatants quantified by fluorometric assay as described in Materials and methods. Controls are untreated HBMEC, Tat.AG represents HBMEC treated with Tat.AG; Tat.B represents HBMEC treated with Tat.B; Tat.B-HI represents HBMEC treated for 48 hours with heat-inactivated Tat.B. HBMEC treated for 48 hours with lipopolysaccharide (LPS) (50 μg/mL) were used as positive controls. Data using HBMEC from human donor 1 (A, E, and I), donor 2 (B, F, and J), and donor 3 (C, G, and K) are shown; and for each donor all experimental conditions were tested in triplicate. Tat.B treatment significantly increased MMP-3 (A–D), MMP-10 (E–H), and MMP-12 (I–L) activities, in comparison with cells treated with Tat.AG, cells treated with heat-inactivated Tat.B, or untreated controls (*P<0.05, **P<0.01, ***P<0.001). P values for Tat.AG-treated cells are in comparison with untreated controls or cells treated with heat-inactivated Tat.B. P value for LPS-treated cells is in comparison with untreated controls, cells treated with Tat.AG, or cells treated with heat-inactivated Tat.B. The MMPs inhibitor tissue inhibitor of metalloproteinase-2 (TIMP2) diminished Tat-induced MMP-3 (D), MMP-10 (H), and MMP-12 (L) activities.