Kruppel-like factor KLF4 facilitates cutaneous wound healing by promoting
fibrocyte generation from myeloid-derived suppressor cells
#MMPMID25581502
Ou L
; Shi Y
; Dong W
; Liu C
; Schmidt TJ
; Nagarkatti P
; Nagarkatti M
; Fan D
; Ai W
J Invest Dermatol
2015[May]; 135
(5
): 1425-1434
PMID25581502
show ga
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.
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