Figure 4.

Knockdown of OPN dampens the recruitment of inflammatory cells and increases neovascularization. (A) Immunohistochemistry (IHC) for myeloperoxidase (neutrophils) and F4/80 (macrophages) or Toluidine blue staining (mast cells) reveals significantly fewer leukocytes in the wound granulation tissue of AS ODN–treated versus control wounds. (B) The number of neutrophils, macrophages, and mast cells at wound sites were quantified for control- (open bars) and OPN AS ODN–treated wounds (filled bars; mean ± SEM; n ≥ 5). (C) Real-time RT-PCR analysis determined the expression of Ccl2, TGFβ1, fibronectin, collagen type1α1, and MMP9 at wound sites, relative to GAPDH, in control ODN (open bars) and OPN AS ODN wounds (filled bars; mean ± SEM; n = 9). (D) CD31/platelet/endothelial cell adhesion molecule 1 IHC reveals blood vessels in control- (left) and OPN AS ODN–treated wounds (right) at 7 d after injury (original wound margins indicated by arrowheads). (E) Graphical representation of the number of vessel lumens in the central wound granulation zone at 7 and 14 d. Bars: (low magnification) 200 μm; (high magnification) 50 μm.

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