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 alpha-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.
journal_name
Circulationjournal_title
Circulationauthors
Otani H,Yamamura T,Nakao Y,Hattori R,Fujii H,Ninomiya H,Kido M,Kawaguchi H,Osako M,Imamura H,Ohta T,Ohkuma Sdoi
10.1161/01.cir.102.suppl_3.iii-269subject
Has Abstractpub_date
2000-11-07 00:00:00pages
III269-74issue
19 Suppl 3eissn
0009-7322issn
1524-4539journal_volume
102pub_type
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