A new role for Nogo as a regulator of vascular remodeling. Nat Med 2004 Apr;10(4):382-8
Date
03/23/2004Pubmed ID
15034570DOI
10.1038/nm1020Scopus ID
2-s2.0-1942518821 (requires institutional sign-in at Scopus site) 222 CitationsAbstract
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.
Author List
Acevedo L, Yu J, Erdjument-Bromage H, Miao RQ, Kim JE, Fulton D, Tempst P, Strittmatter SM, Sessa WCMESH terms used to index this publication - Major topics in bold
AnimalsCell Line
Cell Movement
Endothelium, Vascular
Humans
Muscle, Smooth, Vascular
Myelin Proteins
Nogo Proteins
Protein Isoforms
