Abstract
Several studies have demonstrated potential roles for apelin/APJ signaling in the regulation of oxidative stress associated with ischemia-reperfusion (I/R) injury in several organs. Objective was to assess the role of apelin/APJ signaling in the development of pressure ulcers (PUs) formation after cutaneous I/R injury in mice. We identified that cutaneous I/R injury increased the expression of apelin in the skin at I/R site. Administration of apelin significantly inhibited the formation of PUs. The reductions of blood vessels, hypoxic area and apoptosis in I/R site were inhibited by apelin injection. Oxidative stress signals in OKD48 mice and the expressions of oxidative stress related genes in the skin were suppressed by apelin injection. H2O2-induced intracellular ROS and apoptosis in endothelial cells and fibroblasts were suppressed by apelin in vitro. Furthermore, MM07, biased agonist of APJ, also significantly suppressed the development of PUs after cutaneous I/R, and the inhibitory effect of MM07 on PUs formation was higher than that in apelin. We conclude that apelin/APJ signaling may inhibit cutaneous I/R injury-induced PUs formation by protecting the reduction of vascularity and tissue damage via suppression of oxidative stress. Exogenous application of apelin or MM07 might have therapeutic potentials against the development of PUs.
Highlights
Several studies have demonstrated potential roles for apelin/APJ signaling in the regulation of oxidative stress associated with ischemia-reperfusion (I/R) injury in several organs
Apelin was accumulated around CD31+ endothelial cells in the dermis in the peripheral area of I/R site, and the expression of apelin was increased after reperfusion (Fig. 1B)
These results suggest that apelin expression might be increased by cutaneous I/R-induced hypoxia, and apelin may be mainly produced by I/R affected endothelial cells in the peripheral area of I/R site
Summary
Several studies have demonstrated potential roles for apelin/APJ signaling in the regulation of oxidative stress associated with ischemia-reperfusion (I/R) injury in several organs. Recent studies demonstrated that apelin/APJ signaling prevented oxidative stress, resulting in the inhibition of diabetic microvascular complications[14,15] and the protection of tissue damage caused by I/R injury in kidney, heart and brain[16,17,18]. It has not been elucidated whether apelin/APJ signaling regulates cutaneous I/R injury associated with PUs. we analyzed the role and mechanisms of the regulation of cutaneous I/R-induced PUs formation by apelin/APJ signaling
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