Aurintricarboxylic acid inhibits the nuclear factor-κB-dependent expression of intercellular cell adhesion molecule-1 and endothelial cell selectin on activated human endothelial cells

2011 ◽  
Vol 22 (2) ◽  
pp. 132-139 ◽  
Author(s):  
Ji-Eun Kim ◽  
Sukmook Lee ◽  
Kyou-Sup Han ◽  
Hyun Kyung Kim
Keyword(s):  
Endothelial Cells ◽  
Cell Adhesion ◽  
Endothelial Cell ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Human Endothelial Cells ◽  
Cell Adhesion Molecule 1 ◽  
Intercellular Cell Adhesion Molecule

scholarly journals Dihydrotestosterone Promotes Vascular Cell Adhesion Molecule-1 Expression in Male Human Endothelial Cells via a Nuclear Factor-κB-Dependent Pathway

Endocrinology ◽  
2004 ◽  
Vol 145 (4) ◽  
pp. 1889-1897 ◽  
Author(s):  
Alison K. Death ◽  
Kristine C. Y. McGrath ◽  
Mark A. Sader ◽  
Shirley Nakhla ◽  
Wendy Jessup ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Adhesion ◽  
Cell Adhesion Molecule ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Vascular Cell Adhesion ◽  
Human Endothelial Cells ◽  
Vascular Cell ◽  
Cell Adhesion Molecule 1 ◽  
Dependent Pathway

scholarly journals Human Cytomegalovirus (HCMV) Infection of Endothelial Cells Promotes Naïve Monocyte Extravasation and Transfer of Productive Virus To Enhance Hematogenous Dissemination of HCMV

2006 ◽  
Vol 80 (23) ◽  
pp. 11539-11555 ◽  
Author(s):  
Gretchen L. Bentz ◽  
Marta Jarquin-Pardo ◽  
Gary Chan ◽  
M. Shane Smith ◽  
Christian Sinzger ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Adhesion ◽  
Endothelial Cell ◽  
Human Cytomegalovirus ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Hcmv Infection ◽  
Transendothelial Migration ◽  
Fiber Formation ◽  
Cell Adhesion Molecule 1

ABSTRACT Human cytomegalovirus (HCMV) pathogenesis is dependent on the hematogenous spread of the virus to host tissue. While data suggest that infected monocytes are required for viral dissemination from the blood to the host organs, infected endothelial cells are also thought to contribute to this key step in viral pathogenesis. We show here that HCMV infection of endothelial cells increased the recruitment and transendothelial migration of monocytes. Infection of endothelial cells promoted the increased surface expression of cell adhesion molecules (intercellular cell adhesion molecule 1, vascular cell adhesion molecule 1, E-selectin, and platelet endothelial cell adhesion molecule 1), which were necessary for the recruitment of naïve monocytes to the apical surface of the endothelium and for the migration of these monocytes through the endothelial cell layer. As a mechanism to account for the increased monocyte migration, we showed that HCMV infection of endothelial cells increased the permeability of the endothelium. The cellular changes contributing to the increased permeability and increased naïve monocyte transendothelial migration include the disruption of actin stress fiber formation and the decreased expression of lateral junction proteins (occludin and vascular endothelial cadherin). Finally, we showed that the migrating monocytes were productively infected with the virus, documenting that the virus was transferred to the migrating monocyte during passage through the lateral junctions. Together, our results provide evidence for an active role of the infected endothelium in HCMV dissemination and pathogenesis.

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