title: Genetic Deletion of Galectin-3 Does Not Impair Full-Thickness Excisional Skin Healing.
abstract: Galectin-3 has been linked to the regulation of several molecular processes essential during acute cutaneous wound healing, but a comprehensive study of the role of galectin-3 has yet to be performed. With known roles in macrophage polarization, myofibroblast differentiation, re-epithelialization, and angiogenesis, we hypothesized that genetic deletion of galectin-3 would significantly impair healing of excisional skin wounds in mice. In wild-type mice, galectin-3 expression correlated temporally with the inflammatory phase of healing. Conversely, genetic deletion of galectin-3 did not alter gross wound healing kinetics even though it resulted in delayed re-epithelialization. Wound composition was not altered up to 15 days after wounding in knockout mice, and isolated dermal fibroblast function in vitro was unchanged. We further explored, spatially, the expression of galectin-3 in human chronic wound tissue in relation to the immune cell infiltrate. We show a decreased mRNA and protein abundance in the wound edge tissue, whereas markers of neutrophils, M1 and M2 macrophages are expressed abundantly. Both transforming growth factor-β1 and tumor necrosis factor-α decrease galectin-3 mRNA abundance in chronic wound edge dermal fibroblasts in vitro, providing a potential mechanism for this decreased expression in chronic wounds.
authors.affiliation: Department of Anatomy and Cell Biology, Schulich School of Medicine and Dentistry, Western University, London, Ontario, Canada.
authors.forename: John T
authors.initials: JT
authors.lastname: Walker
authors.affiliation: Department of Anatomy and Cell Biology, Schulich School of Medicine and Dentistry, Western University, London, Ontario, Canada.
authors.forename: Christopher G
authors.initials: CG
authors.lastname: Elliott
authors.affiliation: Division of Vascular Surgery, Schulich School of Medicine and Dentistry, Western University, London, Ontario, Canada.
authors.forename: Thomas L
authors.initials: TL
authors.lastname: Forbes
authors.affiliation: Department of Anatomy and Cell Biology, Schulich School of Medicine and Dentistry, Western University, London, Ontario, Canada; Division of Oral Biology, Schulich School of Medicine and Dentistry, Western University, London, Ontario, Canada. Electronic address: dhamil2@uwo.ca.
authors.forename: Douglas W
authors.initials: DW
authors.lastname: Hamilton
mesh_terms: D000818:Animals; D015153:Blotting, Western; D002478:Cells, Cultured; D016207:Cytokines / Q000494:pharmacology; D004195:Disease Models, Animal; D005347:Fibroblasts / Q000166:cytology / Q000378:metabolism; D037502:Galectin 3 / Q000235:genetics*; D017353:Gene Deletion; D005786:Gene Expression Regulation; D006801:Humans; D051379:Mice; D018345:Mice, Knockout; D011897:Random Allocation; D060888:Real-Time Polymerase Chain Reaction; D012867:Skin / Q000293:injuries* / Q000473:pathology; D053773:Transforming Growth Factor beta1 / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*; D014945:Wound Healing / Q000235:genetics* / Q000502:physiology; D014947:Wounds and Injuries / Q000235:genetics / Q000503:physiopathology
chemical_list: D016207:Cytokines; D037502:Galectin 3; D053773:Transforming Growth Factor beta1; D014409:Tumor Necrosis Factor-alpha