TY - JOUR
T1 - Decorin Inhibits Dermal Mesenchymal Cell Migration and Induces Scar Formation
AU - Takaya, Kento
AU - Aramaki-Hattori, Noriko
AU - Sakai, Shigeki
AU - Okabe, Keisuke
AU - Asou, Toru
AU - Kishi, Kazuo
N1 - Funding Information:
Disclosure: The authors have no financial interest to declare in relation to the content of this article. This work was supported by JSPS KAKENHI (grant number: 19H03815).
Publisher Copyright:
Copyright © 2022 The Authors
PY - 2022/4/11
Y1 - 2022/4/11
N2 - Background: Variations in skin healing capacities are observed during different murine embryonic developmental stages. Through embryonic day 16 (E16), embryos are able to regenerate dermal architecture following flank skin wounding; however, after E17, wounds heal incompletely, inducing scar formation. The regenerative ability of the E16 fetal dermis depends on the migration of dermal mesenchymal cells. Decorin is a small molecule known to affect tissue tensile strength, cell phenotype, and tissue repair, including skin wound healing. In the current study, we evaluated the expression and roles of decorin in wound healing. Methods: Surgical injury was induced at E16 and E17 in ICR mouse embryos. Decorin expression was evaluated in tissue samples from these embryos using immunohistochemistry and reverse transcription quantitative polymerase chain reaction. Cell migration assays were used to evaluate wound healing capability of separated dermal and fascial tissues. Results: Our results showed that decorin exhibited distinct expression patterns during wound healing at E16 versus E17. Additionally, decorin expression altered cell migration in vitro. Dermal and fascial mesenchymal cells were found to exhibit distinct migration patterns concomitant with altered decorin expression. Specifically, decorin inhibited migration and favored scar formation. Conclusion: Decorin expression may contribute to scar formation in the late stage of mouse embryos by inhibiting the migration of dermal mesenchymal cells.
AB - Background: Variations in skin healing capacities are observed during different murine embryonic developmental stages. Through embryonic day 16 (E16), embryos are able to regenerate dermal architecture following flank skin wounding; however, after E17, wounds heal incompletely, inducing scar formation. The regenerative ability of the E16 fetal dermis depends on the migration of dermal mesenchymal cells. Decorin is a small molecule known to affect tissue tensile strength, cell phenotype, and tissue repair, including skin wound healing. In the current study, we evaluated the expression and roles of decorin in wound healing. Methods: Surgical injury was induced at E16 and E17 in ICR mouse embryos. Decorin expression was evaluated in tissue samples from these embryos using immunohistochemistry and reverse transcription quantitative polymerase chain reaction. Cell migration assays were used to evaluate wound healing capability of separated dermal and fascial tissues. Results: Our results showed that decorin exhibited distinct expression patterns during wound healing at E16 versus E17. Additionally, decorin expression altered cell migration in vitro. Dermal and fascial mesenchymal cells were found to exhibit distinct migration patterns concomitant with altered decorin expression. Specifically, decorin inhibited migration and favored scar formation. Conclusion: Decorin expression may contribute to scar formation in the late stage of mouse embryos by inhibiting the migration of dermal mesenchymal cells.
UR - http://www.scopus.com/inward/record.url?scp=85129491745&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85129491745&partnerID=8YFLogxK
U2 - 10.1097/GOX.0000000000004245
DO - 10.1097/GOX.0000000000004245
M3 - Article
AN - SCOPUS:85129491745
SN - 2169-7574
VL - 10
SP - E4245
JO - Plastic and Reconstructive Surgery - Global Open
JF - Plastic and Reconstructive Surgery - Global Open
IS - 4
ER -