Fig. 7.
Fig. 7. Matrix invasion by THP-1 monocytes is inhibited by anti–annexin II. / Cells (4 × 104) were suspended in MSFM and preincubated with either 25 μg/mL monoclonal anti–annexin II IgG (clone Z014, Zymed), monoclonal anti-CD16 IgG, or anti-CD11b IgG. Plasminogen (Plg, 10 μg/mL) was added to the cell suspension and cells were aliquoted into an insert containing a porous (8 μm) polycarbonate membrane previously coated with Matrigel. The insert was placed into a well containing MCP-1 (50 ng/mL) and incubated 24 hours at 37°C. Cells that migrated into the lower well were counted using phase-contrast microscopy. The results of 2 independent experiments containing 3 replicate samples for each condition per experiment were pooled. The 2 experiments were identical except for the control IgG used. For the purposes of presentation and analysis the 2 groups were combined. Data are presented as the mean ± SEM. nIgG indicates normal IgG.

Matrix invasion by THP-1 monocytes is inhibited by anti–annexin II.

Cells (4 × 104) were suspended in MSFM and preincubated with either 25 μg/mL monoclonal anti–annexin II IgG (clone Z014, Zymed), monoclonal anti-CD16 IgG, or anti-CD11b IgG. Plasminogen (Plg, 10 μg/mL) was added to the cell suspension and cells were aliquoted into an insert containing a porous (8 μm) polycarbonate membrane previously coated with Matrigel. The insert was placed into a well containing MCP-1 (50 ng/mL) and incubated 24 hours at 37°C. Cells that migrated into the lower well were counted using phase-contrast microscopy. The results of 2 independent experiments containing 3 replicate samples for each condition per experiment were pooled. The 2 experiments were identical except for the control IgG used. For the purposes of presentation and analysis the 2 groups were combined. Data are presented as the mean ± SEM. nIgG indicates normal IgG.

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