Author/Authors :
Shoji، نويسنده , , Makoto and Sata، نويسنده , , Masataka and Fukuda، نويسنده , , Daiju and Tanaka، نويسنده , , Kimie and Sato، نويسنده , , Takatoshi and Iso، نويسنده , , Yoshitaka and Shibata، نويسنده , , Masayuki and Suzuki، نويسنده , , Hiroshi and Koba، نويسنده , , Shinji and Geshi، نويسنده , , Eiichi and Katagiri، نويسنده , , Takashi، نويسنده ,
Abstract :
Background
ant smooth muscle cells (SMCs) hyperplasia is the major cause of postangioplasty restenosis. We suggested that circulating smooth muscle progenitor cells might contribute to lesion formation after vascular injury.
s
ensively investigated the cellular constituents during neointimal formation after mechanical vascular injury.
s
e wire was inserted into the mouse femoral artery, causing complete endothelial denudation and marked enlargement of the lumen with massive apoptosis of medial SMCs. At 2 h, the injured artery remained dilated with a thin media containing very few cells. A scanning electron microscopy showed fibrin and platelet deposition at the luminal side. One week after the injury, CD45-positive hematopoietic cells accumulated at the luminal side. Those CD45-positive cells gradually disappeared, whereas neointimal hyperplasia was formed with α-smooth muscle actin (SMA) positive cells. Bone marrow cells and peripheral mononuclear cells differentiated into α-SMA-positive cells in the presence of PDGF and basic FGF. Moreover, in bone marrow chimeric mice, bone-marrow-derived cells substantially contributed to neointimal hyperplasia after wire injury.
sion
results suggest that early accumulation of hematopoietic cells may play a role in the pathogenesis of SMC hyperplasia under certain circumstances.
Keywords :
neointima , Injury , Progenitor , Smooth Muscle Cell , Proliferation