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Fig. 6. HOXA3 promotes angiogenesis and wound repair in vivo. (a-c) Effect of HOXA3 treatment on wound closure. Gross appearance of 2.5 cm wounds in Lepr^db/Lepr^db mice, 14 days after treatment with (a) control plasmid, or (b) HOXA3 expression plasmid. (c) Wound closure in control- (pink) and HOXA3-treated (blue) diabetic wounds. Wound area was measured every 7 days following excision of a 2.5 cm diameter wound in Lepr^db/Lepr^db mice. Mice treated with HOXA3 showed a significantly (**P<0.05) greater degree of closure at days 7, 14, 21, 28, 35 and 42 days when compared with closure of control plasmid-treated Lepr^db/Lepr^db wounds (HOXA3, n=10; control, n=10). (d-f) Analysis of vascular density in Lepr^db/Lepr^db wounds 4 days following treatment with control (d) or HOXA3 (e) expression plasmids. 10 µm cryosections were stained with antibodies against CD31 (original magnification x200). (f) Histological scores (±s.d.) of tissue sections from wounds 7 days after administration of control or HOXA3 expression plasmids. Scores include quantification of vascular density, epithelial and fibroblast cell density, collagen deposition, and granulation tissue formation. **P<0.05 compared with score in control cells.

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