Human cytomegalovirus infection induces mRNA expression and secretion of plasminogen inhibitor type-1 in endothelial cells

Abstract

The aim of the study was to investigate whether infection of endothelial cells with human cytomegalovirus (HCMV) perturbs expression and production of plasminogen activator inhibitor type-1 (PAI-1). mRNA expression of PAI-1 was investigated by isolating total RNA from HCMV-infected and control cells, followed by Northern blotting and probing with 32P-labelled PAI-1 probe. Sandwich ELISA was used to investigate PAI-1 production. HCMV induced the expression of PAI-1-mRNA at 2-5 days postinfection (maximum expression was at 3 days postinfection which was 40% higher than control). HCMV also induced secretion of PAI-1 at 2-5 days postinfection. These results indicate that infection of endothelial cells with HCMV disturbs PAI-1 expression and production in these cells.

Review: Viral infections and mechanisms of thrombosis and bleeding

“…There are two mechanisms to consider here. Firstly, increased levels of plasminogen activator inhibitor‐1 have been found in influenza, SARS, VZV, CMV, dengue, and HIV infections [Woodroffe and Kuan, 1998; Kurugol et al, 2000; Koppel et al, 2002; Wills et al, 2002; Klein et al, 2005; Keller et al, 2006; Wu et al, 2006; Sosothikul et al, 2007; Schouten et al, 2010]. In HIV infection, elevated plasminogen activator inhibitor‐1 levels have been shown to be related to the metabolic syndrome and the use of protease inhibitors as part of the antiretroviral therapy [Koppel et al, 2002].…”

Evaluation of the coagulation and inflammatory responses in solid organ transplant recipients and donors

“…While, most early infections are bacterial in nature, disseminated opportunistic viruses, such as cytomegalovirus (CMV), may present with multi‐organ dysfunction in a fashion that is remarkably similar to systemic bacterial infections (7). In vitro data have shown that CMV affects the endothelium directly, i.e., alteration in clotting time and von Willebrand factor production, secretion of plasminogen inhibitor type 1, factor X and thrombin generation, and adhesion of neutrophils, thus leading to pro‐coagulant and inflammatory states (8–15). Clinical evidence for human endothelial injury by CMV is demonstrated by the microvascular involvement in gastro‐intestinal (colitis), cutaneous (purpura), and hematological (thrombotic microangiopathy) diseases (16–22).…”