Dengue virus regulates the expression of hemostasis-related molecules in human vein endothelial cells

Jiang, Zhuhua; Tang, Xi-can; Xiao, Rui; Jiang, Lifang; Chen, Xiaoyin

doi:10.1016/j.jinf.2007.04.351

Cited by 22 publications

(20 citation statements)

References 13 publications

(13 reference statements)

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“…In regards to the coagulation pathway, up-regulation of tissue factor expression by DENV infected cells have been consistently demonstrated while the effects of DENV on endothelial expression of thrombomodulin and PAI-1 have been conflicting(Huerta-Zepeda et al, 2008; Jiang et al, 2007; Yeh et al, 2013) These data are consistent with findings from human studies investigating the coagulation system(Bethell et al, 2001; Sosothikul et al, 2007)…”

Section: Dengue Virus and The Endothelial Barriersupporting

confidence: 79%

Endothelial cells in dengue hemorrhagic fever

Srikiatkhachorn

Kelley

2014

Antiviral Research

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Therapies to prevent or reverse endothelial dysfunction and vascular leak found in dengue hemorrhagic fever (DHF) have not been identified. In this review we summarize dengue viruses and the spectrum of human disease and highlight evidence of endothelial cell dysfunction in DHF based on studies in patients and mouse and tissue culture models. Evidence suggests that both virus antigen and host immune response, can cause endothelial cell dysfunction and weaken endothelial barrier integrity. We suggest possible therapeutic interventions and highlight how therapies targeting altered endothelial function might be evaluated in animal models and in patients with DHF.

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Section: Dengue Virus and The Endothelial Barriersupporting

confidence: 79%

Endothelial cells in dengue hemorrhagic fever

Srikiatkhachorn

Kelley

2014

Antiviral Research

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“…on May 9, 2018. by guest www.bloodjournal.org From virus, 53 nipah virus, 54 herpes simplex virus, 55 or classical swine fever virus 56 can infect EC. The resulting induction of TF expression on EC has been attributed to either viral glycoproteins, the generally toxic insult to the cells by viruses, or via the secondary release of cytokines and other mediators.…”

Section: Discussionmentioning

confidence: 99%

A key role for Toll-like receptor-3 in disrupting the hemostasis balance on endothelial cells

Shibamiya

Hersemeyer

Wöll

et al. 2009

Blood

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“…Previous studies have demonstrated that the expression of t-PA and TM but not plasminogen activator inhibitor 1 mRNA was increased in DV-infected endothelial cells. 19,20 However, it is unclear whether the expression of TM protein is also up-regulated. In this study we demonstrated that DV induced TM expression in endothelial cells and monocytes at both mRNA and protein levels.…”

Section: Discussionmentioning

confidence: 99%