TY - JOUR
T1 - Genetic Deletion of Galectin-3 Does Not Impair Full-Thickness Excisional Skin Healing
AU - Walker, John T.
AU - Elliott, Christopher G.
AU - Forbes, Thomas L.
AU - Hamilton, Douglas W.
N1 - Funding Information:
This work was funded by the Canadian Institutes of Health Research (Operating Grant RN247506) and the Canadian Foundation for Innovation Leaders Opportunity Fund (No. 18742) to DWH. JTW was the recipient of a National Sciences and Engineering Research Council of Canada Alexander Graham Bell Scholarship program.
Publisher Copyright:
© 2016 The Authors
PY - 2016
Y1 - 2016
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=84978069396&partnerID=8YFLogxK
U2 - 10.1016/j.jid.2016.01.014
DO - 10.1016/j.jid.2016.01.014
M3 - Article
C2 - 26829035
AN - SCOPUS:84978069396
SN - 0022-202X
VL - 136
SP - 1042
EP - 1050
JO - Journal of Investigative Dermatology
JF - Journal of Investigative Dermatology
IS - 5
ER -