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Title: Alterations in actin cytoskeletal assembly and junctional protein complexes in human endothelial cells induced by dengue virus infection and mimicry of leukocyte transendothelial migration
Authors: Rattiyaporn Kanlaya
Sa Nga Pattanakitsakul
Supachok Sinchaikul
Shui Tein Chen
Visith Thongboonkerd
Mahidol University
Genomics Research Center, Academia Sinica
National Taiwan University
Faculty of Medicine, Siriraj Hospital, Mahidol University
Keywords: Biochemistry, Genetics and Molecular Biology;Chemistry
Issue Date: 1-May-2009
Citation: Journal of Proteome Research. Vol.8, No.5 (2009), 2551-2562
Abstract: Vascular leakage is a hallmark of severe dengue infection. Although extensive studies have been conducted during the past several decades, the molecular mechanisms underlying vascular leakage in dengue shock syndrome (DSS) remain unclear. We thus performed a proteomics study to characterize responses in human endothelial cells (EA.hy926) after DEN-2 virus infection (MOI = 10). Comparative 2-D PAGE analysis revealed significantly altered abundance levels of 15 proteins, which were successfully identified by quadrupole time-of-flight mass spectrometry (MS) and/or tandem MS (MS/ MS). These altered proteins were involved in several biological processes, for example, mRNA stability/ processing, transcription and translation regulation, molecular chaperoning, oxidative stress response/ regulation, cytoskeletal assembly, protein degradation, and cellular metabolisms. We also performed functional analyses of alterations in actin cytoskeletal assembly and endothelial integrity focusing on adherens junction (VE-cadherin), tight junction (ZO-1) and adhesive molecule (PECAM-1) after 24-h of DEN-2 infection and simulation of transendothelial migration by PECAM-1 cross-linking. Decreased expression and disorganization of the actin-cytoskeleton were observed in the infected cells, whereas the increase in actin stress fibers was found in adjacent noninfected cells. Additionally, a decrease in adhesive protein PECAM-1 was observed. Furthermore, DEN-2 infection caused decreased expression and redistribution of both VE-cadherin and ZO-1, whose changes were enhanced by PECAM-1 engagement. These alterations may potentially be a molecular basis explaining increased endothelial permeability or vascular leakage in DSS. © 2009 American Chemical Society.
ISSN: 15353893
Appears in Collections:Scopus 2006-2010

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