Methylglyoxal-mediated alteration of gene expression in human endothelial cells

2011 ◽  
Vol 5 (3) ◽  
pp. 220-228 ◽  
Author(s):  
Seung Eun Lee ◽  
Hana Yang ◽  
Seong Il Jeong ◽  
Young-Ho Jin ◽  
Cheung-Seog Park ◽  
...  
Keyword(s):  
Gene Expression ◽  
Endothelial Cells ◽  
Human Endothelial Cells

Lipoprotein apheresis of hypercholesterolemic patients mediates vasoprotective gene expression in human endothelial cells

2013 ◽  
Vol 14 (1) ◽  
pp. 107-113 ◽  
Author(s):  
Henning Morawietz ◽  
Winfried Goettsch ◽  
Melanie Brux ◽  
Manja Reimann ◽  
Stefan R. Bornstein ◽  
...  
Keyword(s):  
Gene Expression ◽  
Endothelial Cells ◽  
Human Endothelial Cells ◽  
Lipoprotein Apheresis

scholarly journals Zyxin Mediation of Stretch-Induced Gene Expression in Human Endothelial Cells

2010 ◽  
Vol 107 (7) ◽  
pp. 898-902 ◽  
Author(s):  
Agnieszka Wójtowicz ◽  
Sahana Suresh Babu ◽  
Li Li ◽  
Norbert Gretz ◽  
Markus Hecker ◽  
...  
Keyword(s):  
Gene Expression ◽  
Endothelial Cells ◽  
Human Endothelial Cells

54: Differential gene expression in human endothelial cells after stimulation with sCD40L

2007 ◽  
Vol 26 (2) ◽  
pp. S79-S80
Author(s):  
D. Schuster ◽  
B. Molitor ◽  
B. Parviz ◽  
A. Weber ◽  
A. Barth ◽  
...  
Keyword(s):  
Gene Expression ◽  
Endothelial Cells ◽  
Differential Gene Expression ◽  
Human Endothelial Cells ◽  
Differential Gene

scholarly journals Cytoprotection of human endothelial cells from oxidative stress by polyphenols: the role of gene expression versus direct antioxidant effect

2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Xinyu Wang ◽  
James Bynum ◽  
Salomon Stavchansky ◽  
Michael Dubick ◽  
Robert Hackman ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Endothelial Cells ◽  
Antioxidant Effect ◽  
Human Endothelial Cells

scholarly journals Heparin down-regulates the phorbol ester-induced protein kinase C gene expression in human endothelial cells: enzyme-mediated autoregulation of protein kinase C-α and -δ genes1

FEBS Letters ◽  
1999 ◽  
Vol 449 (2-3) ◽  
pp. 135-140 ◽  
Author(s):  
Gianfranco Pintus ◽  
Bruna Tadolini ◽  
Margherita Maioli ◽  
Anna M. Posadino ◽  
Leonardo Gaspa ◽  
...  
Keyword(s):  
Gene Expression ◽  
Endothelial Cells ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Phorbol Ester ◽  
Human Endothelial Cells ◽  
Kinase C

scholarly journals Toxoplasma gondii Dysregulates Barrier Function and Mechanotransduction Signaling in Human Endothelial Cells

mSphere ◽  
2020 ◽  
Vol 5 (1) ◽  
Author(s):  
Armond L. Franklin-Murray ◽  
Sharmila Mallya ◽  
Allen Jankeel ◽  
Suhas Sureshchandra ◽  
Ilhem Messaoudi ◽  
...  
Keyword(s):  
Gene Expression ◽  
Endothelial Cells ◽  
Shear Stress ◽  
Toxoplasma Gondii ◽  
Molecular Interactions ◽  
Barrier Function ◽  
Hippo Signaling ◽  
Vascular Endothelial ◽  
Human Endothelial Cells ◽  
Content Type

ABSTRACT Toxoplasma gondii can infect and replicate in vascular endothelial cells prior to entering host tissues. However, little is known about the molecular interactions at the parasite-endothelial cell interface. We demonstrate that T. gondii infection of primary human umbilical vein endothelial cells (HUVEC) altered cell morphology and dysregulated barrier function, increasing permeability to low-molecular-weight polymers. T. gondii disrupted vascular endothelial cadherin (VE-cadherin) and β-catenin localization to the cell periphery and reduced VE-cadherin protein expression. Notably, T. gondii infection led to reorganization of the host cytoskeleton by reducing filamentous actin (F-actin) stress fiber abundance under static and microfluidic shear stress conditions and by reducing planar cell polarity. RNA sequencing (RNA-Seq) comparing genome-wide transcriptional profiles of infected to uninfected endothelial cells revealed changes in gene expression associated with cell-cell adhesion, extracellular matrix reorganization, and cytokine-mediated signaling. In particular, genes downstream of Hippo signaling and the biomechanical sensor and transcriptional coactivator Yes-associated protein (YAP) were downregulated in infected endothelial cells. Interestingly, T. gondii infection activated Hippo signaling by increasing phosphorylation of LATS1, leading to cytoplasmic retention of YAP, and reducing YAP target gene expression. These findings suggest that T. gondii infection triggers Hippo signaling and YAP nuclear export, leading to an altered transcriptional profile of infected endothelial cells. IMPORTANCE Toxoplasma gondii is a foodborne parasite that infects virtually all warm-blooded animals and can cause severe disease in individuals with compromised or weakened immune systems. During dissemination in its infected hosts, T. gondii breaches endothelial barriers to enter tissues and establish the chronic infections underlying the most severe manifestations of toxoplasmosis. The research presented here examines how T. gondii infection of primary human endothelial cells induces changes in cell morphology, barrier function, gene expression, and mechanotransduction signaling under static conditions and under the physiological conditions of shear stress found in the bloodstream. Understanding the molecular interactions occurring at the interface between endothelial cells and T. gondii may provide insights into processes linked to parasite dissemination and pathogenesis.

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