Abstract
Cutaneous ischemia-reperfusion (I/R) injury is associated with the early pathogenesis of cutaneous pressure ulcers (PUs). The objective of this study was to investigate the effect of mesenchymal stem cells (MSCs) injection on the formation of PUs after I/R injury and determine the underlying mechanisms. We found that the subcutaneous injection of MSCs into areas of I/R injured skin significantly suppressed the formation of PUs. I/R-induced vascular damage, hypoxia, oxidative DNA damage, and apoptosis were decreased by MSCs injection. Oxidative stress signals detected after I/R in OKD48 (Keap1-dependent oxidative stress detector, No-48-luciferase) mice were decreased by the injection of MSCs. In cultured fibroblasts, MSCs-conditioned medium significantly inhibited oxidant-induced reactive oxygen species (ROS) generation and apoptosis. Furthermore, endoplasmic reticulum (ER) stress signals detected after I/R in ERAI (ER stress-activated indicator) mice were also decreased by the injection of MSCs. These results suggest that the injection of MSCs might protect against the development of PUs after cutaneous I/R injury by reducing vascular damage, oxidative cellular damage, oxidative stress, ER stress, and apoptosis.
Highlights
Because of population aging, the number of patients with pressure ulcers (PUs) is increasing worldwide
We examined the effects of Mesenchymal stem cells (MSCs) on the development of PUs after cutaneous I/R injury in vivo
The wound closure time in control mice was longer than that in MSCs-injected mice (12.8 vs. 11.6 days, P < 0.01). These results suggested that MSCs might protect against the formation of PUs after cutaneous I/R injury
Summary
The number of patients with pressure ulcers (PUs) is increasing worldwide. There is currently no evidence-based early-stage treatment to prevent the development of skin ulcers. Identifying appropriate treatments or techniques to prevent the development of skin ulcers from the initial stage of non-blanchable erythema is essential. Several mechanisms have been identified for promoting wound healing by MSCs, including the enhancement of angiogenesis via the secretion of pro-angiogenic factors, differentiation of MSCs into endothelial cells, pericytes, fibroblasts, and keratinocytes, promotion of M2 macrophages infiltration, recruitment of endogenous stem/progenitor cells, extracellular matrix production and remodeling, and immunosuppressive effects[12,15,16,17,18,19]. There have been no reports demonstrating the effect of MSCs on cutaneous I/R injury and the subsequent formation of skin ulcers. In this study, we examined the effect of MSCs on the acute phase of PUs formation after cutaneous I/R and investigated the underlying mechanisms
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