|Authors||Kraemer R, Baker PJ, Kent KC, Ye Y, Han JJ, Tejada R, Silane M, Upmacis R, Deeb R, Chen Y, Levine DM, Hempstead B|
|Journal||Circulation Volume: 112 Issue: 23 Pages: 3644-53|
|Publish Date||2005 Dec 6|
Accumulation of macrophages and smooth muscle cells in the vascular wall is critical for the development of atherosclerotic lesions. Although much is known about the factors that regulate macrophage recruitment to the vascular wall, the ability of growth factors to regulate smooth muscle cell recruitment in lesion development in vivo is unclear. Our previous studies demonstrated that neurotrophins and their receptors, the Trk receptor tyrosine kinases, are potent chemotactic factors for smooth muscle cells, and the expression of brain-derived neurotrophic factor (BDNF) and its cognate receptor, TrkB, is upregulated in human atherosclerotic lesions.TrkB(/-)/ApoE(-/-) mice.These results suggest that TrkB expression on smooth muscle cells contributes to lesion development in the cholesterol-fed ApoE-null mutant mouse. These data demonstrate, for the first time, a role for the neurotrophin TrkB receptor in atherosclerotic lesion development.