Publication Type
Journal Article
Version
publishedVersion
Publication Date
10-2024
Abstract
Mammals typically heal with fibrotic scars, and treatments to regenerate human skin and hair without a scar remain elusive. We discovered that mice lacking C-X-C motif chemokine receptor 2 (CXCR2 knockout [KO]) displayed robust and complete tissue regeneration across three different injury models: skin, hair follicle, and cartilage. Remarkably, wild-type mice receiving plasma from CXCR2 KO mice through parabiosis or injections healed wounds scarlessly. A comparison of circulating proteins using multiplex ELISA revealed a 24-fold higher plasma level of granulocyte colony stimulating factor (G-CSF) in CXCR2 KO blood. Local injections of G-CSF into wild-type (WT) mouse wound beds reduced scar formation and increased scarless tissue regeneration. G-CSF directly polarized macrophages into an anti-inflammatory phenotype, and both CXCR2 KO and G-CSF-treated mice recruited more anti-inflammatory macrophages into injured areas. Modulating macrophage activation states at early time points after injury promotes scarless tissue regeneration and may offer a therapeutic approach to improve healing of human skin wounds.
Discipline
Cell and Developmental Biology | Econometrics
Research Areas
Econometrics
Publication
Cell Reports
Volume
43
Issue
10
First Page
1
Last Page
20
ISSN
2639-1856
Identifier
10.1016/j.celrep.2024.114742
Publisher
Cell Press
Citation
HUANG, Jianhe; SATI, Satish: MURPHY; SPENCER, Casey A.; RAPP, Emmanuel; PROUTY, Stephen M.; KORTE, Scott; AHART, Olivia; SHENG, Emily; KERSH, Anna E.; LEUNG, Denis; LEUNG, Thomas H.; and LEUNG, Denis H. Y..
Granulocyte colony stimulating factor promotes scarless tissue regeneration. (2024). Cell Reports. 43, (10), 1-20.
Available at: https://ink.library.smu.edu.sg/soe_research/2772
Copyright Owner and License
Authors
Creative Commons License
This work is licensed under a Creative Commons Attribution-NonCommercial-No Derivative Works 4.0 International License.
Additional URL
https://doi.org/10.1016/j.celrep.2024.114742