Imperial College London
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DrAnneBurke-Gaffney

Faculty of Medicine, National Heart & Lung Institute

Lecturer
 
 
 
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a.burke-gaffney

 
 
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Location

 

GSB 311Royal BromptonRoyal Brompton Campus

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Summary

 

Publications

Citation

BibTex format

@article{Burke-Gaffney:1996:10.1111/j.1476-5381.1996.tb16017.x,
author = {Burke-Gaffney, A and Hellewell, PG},
doi = {10.1111/j.1476-5381.1996.tb16017.x},
journal = {Br J Pharmacol},
pages = {1149--1158},
title = {Tumour necrosis factor-alpha-induced ICAM-1 expression in human vascular endothelial and lung epithelial cells: modulation by tyrosine kinase inhibitors.},
url = {http://dx.doi.org/10.1111/j.1476-5381.1996.tb16017.x},
volume = {119},
year = {1996}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - 1. Tumour necrosis factor-alpha (TNF alpha) increases the expression of the adhesion molecule intercellular adhesion molecule-1 (ICAM-1) on cultured endothelial and epithelial cells and modulation of this may be important in controlling inflammation. Activation of tyrosine kinase(s) is known to be involved in the signal transduction pathways of many cytokines. In this study we have investigated the effects of the tyrosine kinase inhibitors, ST638, tyrphostin AG 1288 and genistein, on TNF alpha-induced ICAM-1 expression in human alveolar epithelial (A549) and vascular endothelial (EAhy926) cell lines and also normal human lung microvascular endothelial cells (HLMVEC). 2. ICAM-1 expression on cultured cells was determined by a sensitive enzyme-linked immunosorbant assay (ELISA). Endothelial or epithelial monolayers were exposed to increasing doses of TNF-alpha (0.01-10 ng ml-1), in the presence or absence of either ST638 (3-100 microM), AG 1288 (3-100 microM) or genistein (100 microM) and ICAM-1 expression was measured at 4 and 24 h. Control experiments examined the effect of ST638 on phorbol 12-myristate 13-acetate (PMA, 20 ng ml-1, 4 h)-stimulated ICAM-1 and compared it to that of a specific protein kinase C inhibitor, R031-8220 (10 microM). Also, functional consequences of changes in ICAM-1 expression were assessed by measuring adhesion of 111 In-labelled human neutrophils to EAhy926 endothelial and A549 epithelial monolayers treated with TNF alpha, in the presence or absence of ST638. 3. ST638 caused a concentration-dependent reduction in TNF alpha- (0.1-10 ng ml-1)-induced ICAM-1 on EAhy926 endothelial (at 4 h) and A549 epithelial monolayers (at 4 and 24 h). In contrast, ST638 caused a concentration-dependent increase in TNF alpha- (0.1-10 ng ml-1)-induced ICAM-1 on EAhy926 endothelial cells at 24 h. Similar effects were seen with AG 1288 or genistein. ST638 (100 microM) significantly (P < 0.01) inhibited ICAM-1 expression on HLMVEC endothelial cells induced b
AU  - Burke-Gaffney,A
AU  - Hellewell,PG
DO  - 10.1111/j.1476-5381.1996.tb16017.x
EP  - 1158
PY  - 1996///
SN  - 0007-1188
SP  - 1149
TI  - Tumour necrosis factor-alpha-induced ICAM-1 expression in human vascular endothelial and lung epithelial cells: modulation by tyrosine kinase inhibitors.
T2  - Br J Pharmacol
UR  - http://dx.doi.org/10.1111/j.1476-5381.1996.tb16017.x
UR  - https://www.ncbi.nlm.nih.gov/pubmed/8937718
VL  - 119
ER  -
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