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Atherosclerosis. 2009 Feb;202(2):424-30. doi: 10.1016/j.atherosclerosis.2008.05.049. Epub 2008 Jun 5.

The Nuclear Factor-kappa B p50 subunit is involved in flow-induced outward arterial remodeling.

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Department Experimental Cardiology, University Medical Center Utrecht, The Netherlands.



Outward arterial remodeling is a structural enlargement of the artery that is associated with unstable inflammatory atherosclerotic lesions. Toll-like receptor (Tlr) activation is known as a key pathway in outward arterial remodeling. Tlr activation results in nuclear translocation of the transcription factor Nuclear Factor-kappa B (NF-kappaB) that controls the transcription of many inflammatory genes. The NF-kappaB subunit p50 is generally considered to be an inhibitory subunit of the NF-kappaB complex. We therefore hypothesize that NF-kappaB p50 inhibits outward arterial remodeling.


Carotid artery ligation in mice, induced outward remodeling in contralateral arteries of NF-kappaB p50(-/-) (p50(-/-)) and wild type (WT) arteries. p50(-/-) arteries showed more outward arterial remodeling than WT arteries (19894.0+/-3136.7 microm(2) vs. 6120.7+/-2741.2 microm(2), respectively, P=0.006). In vitro, lipopolysaccharide induced higher cytokine expression levels in p50(-/-) cells compared to WT cells. In vivo, more outward remodeling in p50(-/-) arteries was associated with a decrease in collagen density and an increased influx of macrophages.


The NF-kappaB p50 subunit is involved in outward arterial remodeling. This is probably due to modulation of macrophage influx and adventitial collagen, leading to enhanced flow-induced outward arterial remodeling after targeted deletion of NF-kappaB subunit p50.

[Indexed for MEDLINE]

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