Delayed wound healing in Mac-1-deficient mice is associated with normal monocyte recruitment.
The Mac-1 integrin is an important mediator of migration and inflammatory activation of neutrophils and monocytes. However, the role of Mac-1 in modulating macrophage emigration and activation and its subsequent impact on cutaneous wound healing have not been fully elucidated. To examine the significance of Mac-1 to murine wound healing, we measured epithelialization and granulation tissue formation in partial-thickness ear wounds and full-thickness head wounds, respectively, in Mac-1-deficient mice. Wounds were histologically analyzed at postwounding days 3, 5, and 7. The gap measured between the leading edges of inward-migrating granulation tissue was significantly increased in knockout mice compared with control animals at day 5 (3.8+/-0.3 vs. 2.6+/-0.5 mm; p<0.001) and day 7 (2.2+/-0.4 vs. 0.96+/-0.73 mm; p=0.005). Epithelial gap measurements were also increased in knockout mice vs. wild-type controls at days 3 (0.62+/-0.02 vs. 0.54+/-0.07 mm; p<0.05) and 5 (0.58+/-0.06 vs. 0.39+/-0.08 mm; p<0.001). Immunohistochemistry showed equal numbers of macrophages in knockout and control wounds. These findings show that Mac-1 is required for normal wound healing but that the attenuation in the deposition of granulation tissue and wound epithelialization in Mac-1 knockout mice is not associated with decreased monocyte migration into the wound.
Sisco
Mark
M
Wound Healing Research Laboratory, Division of Plastic Surgery, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA.
Chao
Jerome D
JD
Kim
Injoong
I
Mogford
Jon E
JE
Mayadas
Tanya N
TN
Mustoe
Thomas A
TA
D000818:Animals; D006097:Granulation Tissue / Q000502:physiology; D007120:Immunochemistry; D016177:Macrophage-1 Antigen / Q000502:physiology*; D008264:Macrophages / Q000502:physiology; D051379:Mice; D018345:Mice, Knockout; D009000:Monocytes / Q000502:physiology*; D014945:Wound Healing / Q000187:drug effects*
D016177:Macrophage-1 Antigen