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The Strathprints institutional repository is a digital archive of University of Strathclyde's Open Access research outputs. Strathprints provides access to thousands of Open Access research papers by Strathclyde researchers, including by researchers from the Physical Activity for Health Group based within the School of Psychological Sciences & Health. Research here seeks to better understand how and why physical activity improves health, gain a better understanding of the amount, intensity, and type of physical activity needed for health benefits, and evaluate the effect of interventions to promote physical activity.

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IKKalpha and IKKbeta function in TNFalpha-stimulated adhesion molecule expression in human aortic smooth muscle cells

MacKenzie, C. and Ritchie, E. and Paul, A. and Plevin, R.J. (2007) IKKalpha and IKKbeta function in TNFalpha-stimulated adhesion molecule expression in human aortic smooth muscle cells. Cellular Signalling, 19. pp. 75-80. ISSN 1873-3913

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Abstract

The role of NFκB and it's upstream kinases in regulating adhesion molecule expression in the smooth muscle of the vasculature remains controversial. We therefore examined the effect of blocking the NFκB pathway on TNFα-stimulated ICAM-1 and VCAM-1 expression in primary cultures of human aortic smooth muscle cells using an adenoviral wild-type IκBα construct (Ad.IκBα) and dominant-negative IKKα (Ad.IKKα+/−) and IKKβ (Ad.IKKβ+/−) constructs. Ad.IκBα treatment was found to block NFκB DNA-binding, and thereby completely prevent TNFα-stimulated ICAM-1 and VCAM-1 expression without influencing IKK activity. Ad.IKKβ+/− treatment completely inhibited TNFα-stimulated IKK kinase activity, IκBα degradation and NFκB DNA-binding in addition to completely blocking TNFα-stimulated ICAM-1 and VCAM-1 expression. Ad.IKKα+/− treatment however had no detectable effect on NFκB DNA-binding or ICAM-1 and VCAM-1 expression. Our results demonstrate that TNFα-stimulated ICAM-1 and VCAM-1 expression in human aortic smooth muscle cells is NFκB-dependent, that IKKβ is a suitable target for drug therapy and Ad.IKKβ+/− an effective inhibitor of TNFα-stimulated ICAM-1 and VCAM-1 expression.