Figure 1
Figure 1. Specific plasminogen binding is enhanced by M-CSF treatment of human peripheral blood monocytes and Hoxa9-ER4 cells. Human peripheral blood monocytes were either untreated (A) or treated with 0.44 nM of M-CSF for 8 days (B) and Hoxa9-ER4 cells were either untreated (C) or treated with 20% LADMAC conditioned media (a source of M-CSF) for 2 days (D). The cells were analyzed by dual-color fluorescence-activated cell sorting (FACS) analysis for specific plasminogen binding and CD antigen expression as described.10 Viable (propidium iodide negative and annexin V negative) cells were gated from the nonviable cells. Histogram plots of FITC-plasminogen (left columns) or specific anti-CD antibody binding to viable cells are shown. Gray tracings indicate either FITC-plasminogen or specific anti-CD antibody; black tracings, either FITC-plasminogen + 0.2 M EACA or isotype controls.

Specific plasminogen binding is enhanced by M-CSF treatment of human peripheral blood monocytes and Hoxa9-ER4 cells. Human peripheral blood monocytes were either untreated (A) or treated with 0.44 nM of M-CSF for 8 days (B) and Hoxa9-ER4 cells were either untreated (C) or treated with 20% LADMAC conditioned media (a source of M-CSF) for 2 days (D). The cells were analyzed by dual-color fluorescence-activated cell sorting (FACS) analysis for specific plasminogen binding and CD antigen expression as described.10  Viable (propidium iodide negative and annexin V negative) cells were gated from the nonviable cells. Histogram plots of FITC-plasminogen (left columns) or specific anti-CD antibody binding to viable cells are shown. Gray tracings indicate either FITC-plasminogen or specific anti-CD antibody; black tracings, either FITC-plasminogen + 0.2 M EACA or isotype controls.

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