Abstract
Pressure ulcers (PUs) are serious skin injuries whereby the wound healing process is frequently stalled in the inflammatory phase. Myeloid-derived suppressor cells (MDSCs) accumulate as a result of inflammation and promote cutaneous wound healing by mechanisms that are not fully understood. Recently, MDSCs have been shown to differentiate into fibrocytes, which serve as emerging effector cells that enhance cell proliferation in wound healing. We postulate that in wound healing MDSCs not only execute their immunosuppressive function to regulate inflammation but also stimulate cell proliferation once they differentiate into fibrocytes. In the current study, by using full-thickness and PU mouse models, we found that Kruppel-like factor 4 (KLF4) deficiency resulted in decreased accumulation of MDSCs and fibrocytes, and wound healing was significantly delayed. Conversely, KLF4 activation by the plant-derived product Mexicanin I increased the number of MDSCs and fibrocytes and accelerated the wound healing. Collectively, our study revealed a previously unreported function of MDSCs in cutaneous wound healing and identified Mexicanin I as a potential agent to accelerate PU wound healing.
Original language | English |
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Pages (from-to) | 1425-1434 |
Number of pages | 10 |
Journal | Journal of Investigative Dermatology |
Volume | 135 |
Issue number | 5 |
DOIs | |
State | Published - May 22 2015 |
Bibliographical note
Funding Information:This work was supported by NIH grant (R03AR060987) and ASPIRE-I from University of South Carolina to WA. We thank Dr Udai P. Singh and Mr Kyle McCloskey for technical assistance and Dr Joseph S. Janicki for his editing of the manuscript.
Publisher Copyright:
© 2015 The Society for Investigative Dermatology.
ASJC Scopus subject areas
- Biochemistry
- Molecular Biology
- Dermatology
- Cell Biology