Synergy between thrombin and serotonin in inducing vascular smooth muscle cell proliferation
- 1 December 1999
- journal article
- Published by Elsevier in Journal of Laboratory and Clinical Medicine
- Vol. 134 (6) , 659-667
- https://doi.org/10.1016/s0022-2143(99)90107-5
Abstract
No abstract availableKeywords
This publication has 55 references indexed in Scilit:
- Comparison of the Effects of the Thrombin Inhibitor r-Hirudin in Four Animal Models of Neointima Formation After Arterial InjuryArteriosclerosis, Thrombosis, and Vascular Biology, 1996
- Thrombin receptor activation elicits rapid protein tyrosine phosphorylation and stimulation of the raf-1/MAP kinase pathway preceding delayed mitogenesis in cultured rat aortic smooth muscle cells: evidence for an obligate autocrine mechanism promoting cell proliferation induced by G-protein-coupled receptor agonist.Journal of Clinical Investigation, 1996
- Involvement of Pertussis toxin-sensitive and -insensitive G proteins in α-thrombin signalling on cultured human vascular smooth muscle cellsCellular Signalling, 1996
- Thrombin hypothesis of thrombus generation and vascular lesion formationThe American Journal of Cardiology, 1995
- Involvement of NF-κB Activation in Thrombin-Induced Human Vascular Smooth Muscle Cell ProliferationBiochemical and Biophysical Research Communications, 1994
- Antithrombin III inhibits thrombin-induced proliferation in human arterial smooth muscle cells.Arteriosclerosis and Thrombosis: A Journal of Vascular Biology, 1994
- Thrombin‐induced proliferation and expression of platelet‐derived growth factor‐A chain gene in human vascular smooth muscle cellsFEBS Letters, 1992
- Inhibition of smooth muscle cell proliferation in injured rat arteries. Interaction of heparin with basic fibroblast growth factor.Journal of Clinical Investigation, 1992
- Induction of vascular smooth muscle cell growth by selective activation of the thrombin receptor Effect of heparinFEBS Letters, 1992
- Transforming growth factor-beta activity is potentiated by heparin via dissociation of the transforming growth factor-beta/alpha 2-macroglobulin inactive complex.The Journal of cell biology, 1989