Open AccessTargeted deletion of the inhibitory NF- B p50 subunit in bone marrow-derived cells improves collateral growth after arterial occlusion
Author(s) -
Daphne de Groot,
René Haverslag,
Gérard Pasterkamp,
Dominique P.V. de Kleijn,
Imo E. Hoefer
Publication year - 2010
Publication title -
cardiovascular research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.774
H-Index - 219
eISSN - 1755-3245
pISSN - 0008-6363
DOI - 10.1093/cvr/cvq150
Subject(s) - arteriogenesis , p50 , perfusion , hindlimb , bone marrow , medicine , inflammation , chemistry , ischemia , transcription factor , biochemistry , gene
Adaptive collateral artery growth (arteriogenesis) is an important mechanism to maintain tissue perfusion upon arterial obstruction. Leucocytes and inflammatory mediators play a crucial role in this process. Depletion of the nuclear factor kappa B (NF-κB) p50 subunit modulates inflammatory processes in cardiovascular disease. We hypothesized that NF-κB p50 is a regulator of the inflammatory response after arterial occlusion and subsequent collateral perfusion.