In:
Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 102, No. suppl_3 ( 2000-11-07)
Abstract:
Background —The molecular mechanism of neointimal hyperplasia after vein graft surgery remains elusive. Vacuolar H + -ATPase (V-ATPase) is involved in intracellular trafficking and may play a crucial role in neointimal cell growth. Methods and Results —Cultured human saphenous vein segments developed neointimal formation within 10 days. Neointimal cells were positive for vimentin and α-smooth muscle actin but negative for desmin, which is indicative of myofibroblasts. Those myofibroblasts were found to have originated from periadventitial fibroblasts, which upregulated the expression of 16-kDa proteolipid of V-ATPase before proliferation and phenotypic modulation. Neointimal myofibroblast growth and survival were highly sensitive to inhibition of V-ATPase by bafilomycin A 1 (BA 1 ), because the incorporation of [ 3 H]thymidine into the myofibroblasts was significantly inhibited by nanomolar concentrations of BA 1 and apoptotic cell death was induced by a similar concentration range of BA 1 . In contrast, endothelial cells and differentiated smooth muscle cells were resistant to apoptosis by BA 1 . Conclusions —These results suggest that V-ATPase plays a crucial role in growth and phenotypic modulation of myofibroblasts that contributes to neointimal formation in cultured human saphenous vein.
Type of Medium:
Online Resource
ISSN:
0009-7322
,
1524-4539
DOI:
10.1161/circ.102.suppl_3.III-269
Language:
English
Publisher:
Ovid Technologies (Wolters Kluwer Health)
Publication Date:
2000
detail.hit.zdb_id:
1466401-X
