Targeted Disruption of TGF-β–Smad3 Signaling Leads to Enhanced Neointimal Hyperplasia With Diminished Matrix Deposition in Response to Vascular Injury

The role of transforming growth factor (TGF)-β and its signal in atherogenesis is not fully understood. Here, we examined mice lacking Smad3, a major downstream mediator of TGF-β, to clarify the precise role of Smad3-dependent signaling in vascular response to injury. Femoral arteries were injured i...

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Veröffentlicht in:	Circulation research 2005-04, Vol.96 (8), p.904-912
Hauptverfasser:	Kobayashi, Kazuki, Yokote, Koutaro, Fujimoto, Masaki, Yamashita, Kimihiro, Sakamoto, Akemi, Kitahara, Masaki, Kawamura, Harukiyo, Maezawa, Yoshiro, Asaumi, Sunao, Tokuhisa, Takeshi, Mori, Seijiro, Saito, Yasushi
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Arteriosclerosis - etiology Atherosclerosis (general aspects, experimental research) Biological and medical sciences Blood and lymphatic vessels Bone Marrow Transplantation Cardiology. Vascular system Cell Proliferation Cells, Cultured Collagen Type I - genetics DNA-Binding Proteins - physiology Fundamental and applied biological sciences. Psychology Hyperplasia Matrix Metalloproteinases, Membrane-Associated Medical sciences Metalloendopeptidases - genetics Mice Muscle, Smooth, Vascular - pathology RNA, Messenger - analysis Signal Transduction Smad3 Protein Tissue Inhibitor of Metalloproteinase-1 - genetics Trans-Activators - physiology Transforming Growth Factor beta - physiology Tunica Intima - pathology Vertebrates: cardiovascular system
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