Figure 3.
Figure 3. PGN-induced monocyte TF expression is mediated by cell surface and internalization-dependent signaling. (A) The frequency of PGN-induced procoagulant monocytes is reduced by the phagocytic inhibitor cytoD and/or Syk inhibition proximally downstream of FcγR signaling with piceatannol (PCT). (B) TF fluorescence intensity in PGN-stimulated monocytes is sensitive to cytoD and/or PCT. (C) Pairwise normalization of monocyte TF expression after PGN stimulation in the presence of cytoD and/or PCT. (A-C) Similar results were obtained in the presence of autologous donor serum (AHS; blue squares) or fetal bovine serum supplemented with human IgG (FBS + IgG; red circles). (D) Comparison of relative sensitivity to cytoD and/or PCT of PGN-induced paired procoagulant (TF+) and proinflammatory (TNF-α+) monocyte responses. Individual data represent inducible marker expression, either TF or TNF-α, in the presence of inhibitors after normalization to PGN-induced expression in the absence of pharmacologic inhibitors. Horizontal bars depict median and IQR in all panels. Graphic representation of comparisons between groups has been omitted for clarity and is summarized in text.

PGN-induced monocyte TF expression is mediated by cell surface and internalization-dependent signaling. (A) The frequency of PGN-induced procoagulant monocytes is reduced by the phagocytic inhibitor cytoD and/or Syk inhibition proximally downstream of FcγR signaling with piceatannol (PCT). (B) TF fluorescence intensity in PGN-stimulated monocytes is sensitive to cytoD and/or PCT. (C) Pairwise normalization of monocyte TF expression after PGN stimulation in the presence of cytoD and/or PCT. (A-C) Similar results were obtained in the presence of autologous donor serum (AHS; blue squares) or fetal bovine serum supplemented with human IgG (FBS + IgG; red circles). (D) Comparison of relative sensitivity to cytoD and/or PCT of PGN-induced paired procoagulant (TF+) and proinflammatory (TNF-α+) monocyte responses. Individual data represent inducible marker expression, either TF or TNF-α, in the presence of inhibitors after normalization to PGN-induced expression in the absence of pharmacologic inhibitors. Horizontal bars depict median and IQR in all panels. Graphic representation of comparisons between groups has been omitted for clarity and is summarized in text.

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