Sepsis decreases lung SVEP1 expression in a murine model

Abstract

Background: Genome-wide association studies have identified sushi, von Willebrand factor type A, EGF, and pentraxin domain-containing 1 (SVEP1) polymorphism as a genetic risk factor for sepsis, as well as acute coronary syndrome. However, research on the role of SVEP1 in systemic inflammation, such as surgical invasion and sepsis, remains insufficient. Therefore, we investigated SVEP1 gene expression and protein levels after surgical invasion and sepsis in mice. Methods: We compared the gene expression and protein levels of SVEP1 between the control (no surgery), sham operation model, and sepsis model with cecal ligation and puncture in mice. Samples were collected at 2, 6, and 24 h after surgery. Results: The lungs had high gene expression and protein production of SVEP1 at baseline. Sham operation and sepsis decreased SVEP1 gene expression in the lungs immediately after stimulation. Furthermore, sepsis significantly downregulated the gene expression compared with sham operation. Flow cytometric analysis showed that mice with sepsis had a significantly decreased percentage of CD31high / SVEP1high and lymphatic vessel endothelial receptor 1 (LYVE-1)high / SVEP1high cells and an increased percentage of CD45.2high / SVEP1high cells. Conclusions: Sepsis decreased SVEP1 gene expression in the lungs. Mice with sepsis had a decreased percentage of SVEP1high vascular and lymphatic endothelial cells and an increased percentage of SVEP1high hematopoietic cells.