Authors: | Acevedo, L.; Yu, J.; Erdjument-Bromage, H.; Miao, R. Q.; Kim, J. E.; Fulton, D.; Tempst, P.; Strittmatter, S. M.; Sessa, W. C. |
Article Title: | A new role for Nogo as a regulator of vascular remodeling |
Abstract: | Although Nogo-A has been identified in the central nervous system as an inhibitor of axonal regeneration, the peripheral roles of Nogo isoforms remain virtually unknown. Here, using a proteomic analysis to identify proteins enriched in caveolae and/or lipid rafts (CEM/LR), we show that Nogo-B is highly expressed in cultured endothelial and smooth muscle cells, as well as in intact blood vessels. The N terminus of Nogo-B promotes the migration of endothelial cells but inhibits the migration of vascular smooth muscle (VSM) cells, processes necessary for vascular remodeling. Vascular injury in Nogo-A/B-deficient mice promotes exaggerated neointimal proliferation, and adenoviral-mediated gene transfer of Nogo-B rescues the abnormal vascular expansion in those knockout mice. Our discovery that Nogo-B is a regulator of vascular homeostasis and remodeling broadens the functional scope of this family of proteins. |
Keywords: | nonhuman; cell proliferation; protein analysis; animal cell; mouse; animals; smooth muscle fiber; cell line; animal experiment; animal model; cell strain cos7; proteomics; gene transfer; animalia; endothelium cell; cell culture; endothelium, vascular; rat; blood vessel injury; cell migration; cell movement; adenovirus vector; protein isoforms; knockout mouse; adenoviridae; intima; muscle, smooth, vascular; protein nogo; caveola; humans; priority journal; article; protein nogo a; myelin proteins |
Journal Title: | Nature Medicine |
Volume: | 10 |
Issue: | 4 |
ISSN: | 1078-8956 |
Publisher: | Nature Publishing Group |
Date Published: | 2004-04-01 |
Start Page: | 382 |
End Page: | 388 |
Language: | English |
DOI: | 10.1038/nm1020 |
PROVIDER: | scopus |
PUBMED: | 15034570 |
DOI/URL: | |
Notes: | Nat. Med. -- Cited By (since 1996):117 -- Export Date: 16 June 2014 -- CODEN: NAMEF -- Source: Scopus |