scholarly journals Methicillin-resistant Staphylococcus aureus enhances alveolar epithelial cell permeability through vascular endothelial growth factor and cytoskeletal disruption

Critical Care ◽  
2008 ◽  
Vol 12 (Suppl 5) ◽  
pp. P38 ◽  
Author(s):  
Kamna Bansal ◽  
Rhykka Connelly ◽  
Daniel Traber ◽  
Perenlei Enkhbaatar
Keyword(s):  
Staphylococcus Aureus ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Methicillin Resistant Staphylococcus Aureus ◽  
Alveolar Epithelial Cell ◽  
Cell Permeability ◽  
Vascular Endothelial ◽  
Alveolar Epithelial ◽  
Endothelial Growth Factor ◽  
Cytoskeletal Disruption

scholarly journals Andes Virus Disrupts the Endothelial Cell Barrier by Induction of Vascular Endothelial Growth Factor and Downregulation of VE-Cadherin

2010 ◽  
Vol 84 (21) ◽  
pp. 11227-11234 ◽  
Author(s):  
Punya Shrivastava-Ranjan ◽  
Pierre E. Rollin ◽  
Christina F. Spiropoulou
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Growth Factor ◽  
Virus Replication ◽  
Cell Permeability ◽  
Hantavirus Infection ◽  
Vascular Endothelial ◽  
Andes Virus ◽  
Endothelial Growth Factor

ABSTRACT Hantavirus pulmonary syndrome (HPS) and hemorrhagic fever with renal syndrome (HFRS) are severe diseases associated with hantavirus infection. High levels of virus replication occur in microvascular endothelial cells but without a virus-induced cytopathic effect. However, virus infection results in microvascular leakage, which is the hallmark of these diseases. VE-cadherin is a major component of adherens junctions, and its interaction with the vascular endothelial growth factor (VEGF) receptor, VEGF-R2, is important for maintaining the integrity of the endothelial barrier. Here we report that increased secreted VEGF and concomitant decreased VE-cadherin are seen at early times postinfection of human primary lung endothelial cells with an HPS-associated hantavirus, Andes virus. Furthermore, active virus replication results in increased permeability and loss of the integrity of the endothelial cell barrier. VEGF binding to VEGF-R2 is known to result in dissociation of VEGF-R2 from VE-cadherin and in VE-cadherin activation, internalization, and degradation. Consistent with this, we showed that an antibody which blocks VEGF-R2 activation resulted in inhibition of the Andes virus-induced VE-cadherin reduction. These data implicate virus induction of VEGF and reduction in VE-cadherin in the endothelial cell permeability seen in HPS and suggest potential immunotherapeutic targets for the treatment of the disease.

scholarly journals Nemo-like kinase regulates the expression of vascular endothelial growth factor (VEGF) in alveolar epithelial cells

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Hengning Ke ◽  
Katarzyna Chmielarska Masoumi ◽  
Kristofer Ahlqvist ◽  
Michael J. Seckl ◽  
Kristina Rydell-Törmänen ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Epithelial Cells ◽  
Alveolar Epithelial Cells ◽  
Vascular Endothelial ◽  
Alveolar Epithelial ◽  
Endothelial Growth Factor
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