To proliferate, vascular smooth muscle cells first convert from a contractile to a synthetic phenotype. Earlier studies indicate that this process is supported by fibronectin and accelerated by platelet-derived growth factor (PDGF). Here, the mechanisms in this transition were further explored. Isolated @entity35 aortic smooth muscle cells were treated with @entity69735 , a PDGF receptor @entity4149 kinase inhibitor, and @entity2307 , a @entity7425 3-kinase inhibitor. Electron microscopy did not show any effect on the reorganization of the cells during the first days in culture, i.e. the loss of actin filaments and the formation of a large secretory apparatus. Conversely, both drugs caused @entity1184 of the Golgi complex, with large and partly vacuolized cisternal stacks. Nevertheless, a juxtanuclear staining pattern for the Golgi enzyme mannosidase II, the coat protein @entity69736 , and the PDGF beta-receptor was retained. Moreover, the serum-induced proliferation of the cells was blocked. These findings suggest that signaling via PDGF receptor @entity4149 kinases and @entity7425 3-kinases is not necessary for the shift of the smooth muscle cells from a contractile to a synthetic phenotype. On the other hand, these enzymes apparently carry out important functions in the control of intracellular membrane traffic and cell division.

XXXX and wortmannin perturb the Golgi complex and block proliferation of vascular smooth muscle cells.

@entity7425 :: ('CHEBI:18179', 'Chemical') :: ['phosphoinositide'] @entity69735 :: ('MESH:C406122', 'Chemical') :: ['tyrphostin A9'] @entity1184 :: ('MESH:D006984', 'Disease') :: ['hypertrophy'] @entity2307 :: ('MESH:C009687', 'Chemical') :: ['wortmannin'] @entity35 :: ('10116', 'Species') :: ['rat'] @entity69736 :: ('60384(Tax:10116)', 'Gene') :: ['beta-COP'] @entity4149 :: ('D014443', 'Chemical') :: ['tyrosine']
@entity69735 :: (MESH:C406122,Chemical) :: ['Tyrphostin A9']
