Open AccessATTENUATION OF CYTOMEGALOVIRUS-INDUCED ENDOTHELIAL INTERCELLULAR ADHESION MOLECULE-1 mRNA/PROTEIN EXPRESSION AND T LYMPHOCYTE ADHESION BY A 2′-O-METHOXYETHYL ANTISENSE OLIGONUCLEOTIDE1,2
Author(s) -
Knight Da,
Briggs Br,
Bennett Cf,
Nagaradona Harindranath,
Waldman Wj,
Sedmak Dd
Publication year - 2000
Publication title -
transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.45
H-Index - 204
eISSN - 1534-6080
pISSN - 0041-1337
DOI - 10.1097/00007890-200002150-00019
Subject(s) - intercellular adhesion molecule 1 , icam 1 , intracellular , biology , endothelial activation , cell adhesion molecule , lymphocyte , oligonucleotide , intercellular adhesion molecule , inflammation , messenger rna , integrin , lymphocyte function associated antigen 1 , sense (electronics) , microbiology and biotechnology , cell adhesion , immunology , chemistry , cell , dna , biochemistry , gene
Intercellular adhesion molecule-1 (ICAM-1) is strongly induced under inflammatory conditions associated with allograft rejection, thereby promoting leukocyte recruitment and activation at the site of inflammation. Enhancement of ICAM-1 expression can also be the result of viral infection, in particular human cytomegalovirus (CMV), a frequent source of complications in the transplant recipient. In vitro studies have shown that CMV infection of endothelial cells (EC) results in the direct enhancement of ICAM-1 expression and consequent leukocyte adhesion/activation suggesting mechanisms by which CMV exacerbates graft vascular disease. Although treatment of EC with ICAM-1-specific antisense oligonucleotides has been shown to attenuate ICAM-1 induction under simulated inflammatory conditions (i.e., TNF-alpha), no studies have addressed their effectiveness on virally-induced ICAM-1 expression.