Vascular endothelial ERp72 is involved in the inflammatory response in a rat model of skeletal muscle injury.

Abstract

The vascular inflammatory response involves the coordinated action of a large network of molecular mediators and culminates in the transmigration of leukocytes into the site of inflammation. Inflammatory mediators include a variety of protein families, including adhesion molecules such as integrins and members of the immunoglobulin superfamily, as well as other cytokines and chemokines. In this study, a rat model of traumatic skeletal muscle injury was used to demonstrate endoplasmic reticulum resident protein 72 (ERp72) overexpression in the early phase of the inflammatory response that follows skeletal muscle injury. Reverse transcription-quantitative PCR, western blotting, dual-labeling immunohistochemistry and immunofluorescence experiments confirmed that ERp72 was expressed on the endothelial cells of blood vessels present at the injured area. In addition, a cell-based neutrophil adhesion assay indicated that a polyclonal antibody specific for ERp72 significantly reduced adhesion of neutrophils to activated human umbilical vein endothelial cells (35% reduction). These data suggested that ERp72 expression on vascular endothelial cells may play a role in skeletal muscle inflammation and could be considered as a target for the modulation of leukocyte-endothelial cell interactions in an inflammatory setting.