Figure 5
Figure 5. CSF-1 inhibition mostly depletes BMDCs in wound healing. (A-B) Quantitative PCR analysis for csf-1 and csfr-1 (n = 4). (C) The procedure for CSF-1 inhibition combined with the dorsal excisional wound model and the GFP-BM chimeric experiment. (D-E) Immunohistochemistry for dorsal skin wounds of PBS- or Ki20227-injected GFP-BM chimeric mice. Ki20227 treatment depleted a large number of GFP+ BMDCs in the wound site. (F) Quantification of the GFP+ cells (n = 3). (G-H) Immunohistochemistry for dorsal skin wounds of control IgGs- or AFS98-injected GFP-BM chimeric mice. AFS98 treatment depleted a large number of GFP+ BMDCs in the wound site. (I) Quantification of the GFP+ cells (n = 3). Bars represent 100 μm. *P < .05, **P < .01.

CSF-1 inhibition mostly depletes BMDCs in wound healing. (A-B) Quantitative PCR analysis for csf-1 and csfr-1 (n = 4). (C) The procedure for CSF-1 inhibition combined with the dorsal excisional wound model and the GFP-BM chimeric experiment. (D-E) Immunohistochemistry for dorsal skin wounds of PBS- or Ki20227-injected GFP-BM chimeric mice. Ki20227 treatment depleted a large number of GFP+ BMDCs in the wound site. (F) Quantification of the GFP+ cells (n = 3). (G-H) Immunohistochemistry for dorsal skin wounds of control IgGs- or AFS98-injected GFP-BM chimeric mice. AFS98 treatment depleted a large number of GFP+ BMDCs in the wound site. (I) Quantification of the GFP+ cells (n = 3). Bars represent 100 μm. *P < .05, **P < .01.

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