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Specific disruption of Lnk in murine endothelial progenitor cells promotes dermal wound healing via enhanced vasculogenesis, activation of myofibroblasts, and suppression of inflammatory cell recruitment.

Specific disruption of Lnk in murine endothelial progenitor cells promotes dermal wound healing via enhanced vasculogenesis, activation of myofibroblasts, and suppression of inflammatory cell recruitment.
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Lee JH, Ji ST, Kim J, Takaki S, Asahara T, Hong YJ, Kwon SM,


Lee JH, Ji ST, Kim J, Takaki S, Asahara T, Hong YJ, Kwon SM, (click to view)

Lee JH, Ji ST, Kim J, Takaki S, Asahara T, Hong YJ, Kwon SM,

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Stem cell research & therapy 2016 Oct 287(1) 158
Abstract
BACKGROUND
Although endothelial progenitor cells (EPCs) contribute to wound repair by promoting neovascularization, the mechanism of EPC-mediated wound healing remains poorly understood due to the lack of pivotal molecular targets of dermal wound repair.

METHODS AND RESULTS
We found that genetic targeting of the Lnk gene in EPCs dramatically enhances the vasculogenic potential including cell proliferation, migration, and tubule-like formation as well as accelerates in vivo wound healing, with a reduction in fibrotic tissue and improved neovascularization via significant suppression of inflammatory cell recruitment. When injected into wound sites, Lnk (-/-) EPCs gave rise to a significant number of new vessels, with remarkably increased survival of transplanted cells and decreased recruitment of cytotoxic T cells, macrophages, and neutrophils, but caused activation of fibroblasts in the wound-remodeling phase. Notably, in a mouse model of type I diabetes, transplanted Lnk (-/-) EPCs induced significantly better wound healing than Lnk (+/+) EPCs did.

CONCLUSIONS
The specific targeting of Lnk may be a promising EPC-based therapeutic strategy for dermal wound healing via improvement of neovascularization but inhibition of excessive inflammation as well as activation of myofibroblasts during dermal tissue remodeling.

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