We report here that degraded type I collagen fragments activate NF-kappa B via phosphorylation and degradation of I kappa B alpha in human vascular smooth muscle cells (SMC) via alpha v beta 3 integrins. Simultanously, collagen fragments induce the expression of IAPs in a NF-kappa B-dependend manner. Inhibition of NF-kappa B results in suppression of IAP upregulation and induces apoptosis. These data identify a novel protective mechanism for SMC against apoptosis under conditions of enhanced extracellular matrix (ECM) degradation as e.g. in the atherosclerotic lesion.
Degraded collagen fragments activate NF-kappa B and protect human smooth muscle cells against apoptosis through induction of inhibitor of apoptosis proteins (IAPs) / K. von Wnuck Lipinski, N. Ferri, B. Levkau - In: Cardio-Visionen : Junge Exzellenz in der Kardiovaskulären Forschung / O. Schober, J. Schrader. - Paderborn : Ferdinand Schoningh, 2005. - ISBN 9783506729682. - pp. 51-52 (( convegno Symposium of the Nordrhein-Westfalischen-Akademie-der-Wissenschaften tenutosi a Dusseldorf nel 2004.
Degraded collagen fragments activate NF-kappa B and protect human smooth muscle cells against apoptosis through induction of inhibitor of apoptosis proteins (IAPs)
N. FerriSecondo
;
2005
Abstract
We report here that degraded type I collagen fragments activate NF-kappa B via phosphorylation and degradation of I kappa B alpha in human vascular smooth muscle cells (SMC) via alpha v beta 3 integrins. Simultanously, collagen fragments induce the expression of IAPs in a NF-kappa B-dependend manner. Inhibition of NF-kappa B results in suppression of IAP upregulation and induces apoptosis. These data identify a novel protective mechanism for SMC against apoptosis under conditions of enhanced extracellular matrix (ECM) degradation as e.g. in the atherosclerotic lesion.Pubblicazioni consigliate
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