Journal
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
Volume 30, Issue 12, Pages 2458-2466Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/ATVBAHA.110.215467
Keywords
angioplasty; pharmacology; vascular biology; NEMO binding domain peptide; nuclear factor-kappa B
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Funding
- Italian Government [PRIN2007, 2007LTAJMA_001]
- Regione Campania [L.R. n. 5/2002-Ann]
- Biotechnology and Biological Sciences Research Council (BBSRC)
- British Pharmacological Society (BPS)
- Medical Research Council (MRC)
- Knowledge Transfer Network (KTN)
- Scottish Funding Council (SFC)
- BBSRC [BB/E527071/1] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/E527071/1] Funding Source: researchfish
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Objective-The activation of nuclear factor-kappa B (NF-kappa B) is a crucial step in the arterial wall's response to injury. The identification and characterization of the NF-kappa B essential modulator-binding domain (NBD) peptide, which can block the activation of the I kappa B kinase complex, have provided an opportunity to selectively abrogate the inflammation-induced activation of NF-kappa B. The aim of the present study was to evaluate the effect of the NBD peptide on neointimal formation. Methods and Results-In the rat carotid artery balloon angioplasty model, local treatment with the NBD peptide (300 mu g/site) significantly reduced the number of proliferating cells at day 7 (by 40%; P < 0.01) and reduced injury-induced neointimal formation (by 50%; P < 0.01) at day 14. These effects were associated with a significant reduction of NF-kappa B activation and monocyte chemotactic protein-1 expression in the carotid arteries of rats treated with the peptide. In addition, the NBD peptide (0.01 to 1 mu mol/L) reduced rat smooth muscle cell proliferation, migration, and invasion in vitro. Similar results were observed in apolipoprotein E-/- mice in which the NBD peptide (150 mu g/site) reduced wire-induced neointimal formation at day 28 (by 47%; P < 0.01). Conclusion-The NBD peptide reduces neointimal formation and smooth muscle cell proliferation/migration, both effects associated with the inhibition of NF-kappa B activation. (Arterioscler Thromb Vasc Biol. 2010;30:2458-2466.)
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