Linked Life Data

15805138

Source:http://linkedlifedata.com/resource/pubmed/id/15805138

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2005-7-8
pubmed:abstractText
Expression of cell adhesion molecule in endothelial cells upon activation by human immunodeficiency virus (HIV) infection is associated with the development of atherosclerotic vasculopathy. We postulated that induction of vascular cell adhesion molecule-1 (VCAM-1) by HIV-1 Tat protein in endothelial cells might represent an early event that could culminate in inflammatory cell recruitment and vascular injury. We determined the role of HIV-1 Tat protein in VCAM-1 expression in human pulmonary artery endothelial cells (HPAEC). HIV-1 Tat protein treatment significantly increased cell-surface expression of VCAM-1 in HPAEC. Consistently, mRNA expression of VCAM-1 was also increased by HIV-1 Tat protein as measured by RT-PCR. HIV-1 Tat protein-induced VCAM-1 expression was abolished by the NF-kappaB inhibitor pyrrolidine dithiocarbamate (PDTC) and the p38 MAPK inhibitor SB-203580. Furthermore, HIV-1 Tat protein enhanced DNA binding activity of NF-kappaB, facilitated nuclear translocation of NF-kappaB subunit p65, and increased production of reactive oxygen species (ROS). Similarly to VCAM-1 expression, HIV-1 Tat protein-induced NF-kappaB activation and ROS generation were abrogated by PDTC and SB-203580. These data indicate that HIV-1 Tat protein is able to induce VCAM-1 expression in HPAEC, which may represent a pivotal early molecular event in HIV-induced vascular/pulmonary injury. These data also suggest that the molecular mechanism underlying the HIV-1 Tat protein-induced VCAM-1 expression may involve ROS generation, p38 MAPK activation, and NF-kappaB translocation, which are the characteristics of pulmonary endothelial cell activation.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1040-0605
pubmed:author
pubmed:issnType
Print
pubmed:volume
289
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
L252-60
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:15805138-Antioxidants, pubmed-meshheading:15805138-Cell Nucleus, pubmed-meshheading:15805138-Cells, Cultured, pubmed-meshheading:15805138-Endothelium, Vascular, pubmed-meshheading:15805138-Enzyme Activation, pubmed-meshheading:15805138-Gene Expression, pubmed-meshheading:15805138-Gene Products, tat, pubmed-meshheading:15805138-Humans, pubmed-meshheading:15805138-NF-kappa B, pubmed-meshheading:15805138-Proline, pubmed-meshheading:15805138-Protein Transport, pubmed-meshheading:15805138-Pulmonary Artery, pubmed-meshheading:15805138-RNA, Messenger, pubmed-meshheading:15805138-Reactive Oxygen Species, pubmed-meshheading:15805138-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:15805138-Signal Transduction, pubmed-meshheading:15805138-Thiocarbamates, pubmed-meshheading:15805138-Vascular Cell Adhesion Molecule-1, pubmed-meshheading:15805138-p38 Mitogen-Activated Protein Kinases
pubmed:year
2005
pubmed:articleTitle
HIV-1 Tat protein-induced VCAM-1 expression in human pulmonary artery endothelial cells and its signaling.
pubmed:affiliation
Department of Medicine, Tulane Univ. School of Medicine, New Orleans, LA 70112-2699, USA. kliu@tulane.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural