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Delayed wound healing in Mac‐1–deficient mice is associated with normal monocyte recruitment
Author(s) -
Sisco Mark,
Chao Jerome D.,
Kim Injoong,
Mogford Jon E.,
Mayadas Tanya N.,
Mustoe Thomas A.
Publication year - 2007
Publication title -
wound repair and regeneration
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.847
H-Index - 109
eISSN - 1524-475X
pISSN - 1067-1927
DOI - 10.1111/j.1524-475x.2007.00264.x
Subject(s) - granulation tissue , wound healing , knockout mouse , monocyte , macrophage , immunohistochemistry , andrology , medicine , chemistry , pathology , immunology , receptor , in vitro , biochemistry
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.