Abstract
Our previous work indicated that TWEAK is associated with various types of cutaneous vasculitis (CV). Herein, we investigate the effects of TWEAK on vascular injury and adhesion molecule expression in CV mice. We showed that TWEAK priming in mice induced a local CV. Furthermore, TWEAK priming also increased the extravasation of FITC-BSA, myeloperoxidase activity and the expression of E-selectin and ICAM-1. Conversely, TWEAK blockade ameliorated the LPS-induced vascular damage, leukocyte infiltrates and adhesion molecules expression in LPS-induced CV. In addition, TWEAK treatment of HDMECs up-regulated E-selectin and ICAM-1 expression at both mRNA and protein levels. TWEAK also enhanced the adhesion of PMNs to HDMECs. Finally, western blot data revealed that TWEAK can induce phosphorylation of p38, JNK and ERK in HDMECs. These data suggest that TWEAK acted as an inducer of E-selectin and ICAM-1 expression in CV mice and HDMECs, may contribute to the development of CV.
Highlights
Vasculitis is characterized by an inflammatory reaction directed at vessels, in which destruction of the wall of blood vessels by leukocytes is the primary event
We showed that Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and factorinducible 14 (Fn14) was expressed on endothelial cells in the skin from control mice
Data suggests that TWEAK and Fn14 might be associated with LPS-induced cutaneous vasculitis (CV)
Summary
Vasculitis is characterized by an inflammatory reaction directed at vessels, in which destruction of the wall of blood vessels by leukocytes is the primary event. Inflammatory injury to blood vessel walls plays a crucial role in the development of CV. It has been reported that TWEAK/Fn14 interaction plays a crucial role in many types of pathologic inflammatory disorders, such as atherosclerosis [5], diabetes [6], chronic kidney disease [7], cardiac dysfunction and failure [8] and SLE [9]. In these conditions, endothelial cells are the initial sites of inflammatory damage
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