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Murine Dermal Fibroblast Isolation by FACS
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Kruppel-like factor KLF4 facilitates cutaneous wound healing by promoting fibrocyte generation from myeloid-derived

Lingling Ou1,2, Ying Shi1,3, Wenqi Dong2

  • 1Department of Pathology, Microbiology and Immunology, University of South Carolina School of Medicine, Columbia, SC, USA.

The Journal of Investigative Dermatology
|January 13, 2015
PubMed

Insights

Myeloid-derived suppressor cells (MDSCs) promote wound healing by differentiating into fibrocytes. Activating KLF4 with Mexicanin I increased MDSCs and fibrocytes, accelerating pressure ulcer healing.

Area of Science:

  • Immunology
  • Dermatology
  • Regenerative Medicine

Background:

  • Pressure ulcers (PUs) exhibit delayed wound healing, often stalled in the inflammatory phase.
  • Myeloid-derived suppressor cells (MDSCs) accumulate during inflammation and influence cutaneous wound healing.
  • MDSCs can differentiate into fibrocytes, which are implicated in enhancing cell proliferation during healing.

Purpose of the Study:

  • To investigate the role of MDSCs in wound healing, specifically their differentiation into fibrocytes.
  • To explore the function of Kruppel-like factor 4 (KLF4) in regulating MDSC and fibrocyte accumulation.
  • To assess the therapeutic potential of Mexicanin I in accelerating pressure ulcer healing.

Main Methods:

  • Utilized full-thickness and pressure ulcer mouse models.
  • Investigated the effects of KLF4 deficiency on MDSC and fibrocyte accumulation and wound healing.
  • Examined the impact of Mexicanin I, a plant-derived product, on MDSC and fibrocyte levels and wound closure.

Main Results:

  • KLF4 deficiency led to reduced MDSC and fibrocyte accumulation, significantly delaying wound healing.
  • Activation of KLF4 by Mexicanin I increased the number of MDSCs and fibrocytes.
  • Mexicanin I treatment accelerated the wound healing process in the studied models.

Conclusions:

  • MDSCs play a significant, previously unreported role in cutaneous wound healing through their immunosuppressive and proliferative functions.
  • KLF4 is a key regulator of MDSC and fibrocyte accumulation in wound healing.
  • Mexicanin I demonstrates potential as a therapeutic agent for accelerating pressure ulcer healing by modulating MDSCs and fibrocytes.

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