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Cell migration is an integral part of the development of intimal hyperplasia, and proteases are pivotal components in the process. Cell migration in response to urokinase is mediated through the aminoterminal fragment (ATF) of the protein. This study examines the role of NAD(P)H oxidase during epidermal growth factor receptor (EGFR) transactivation by ATF in human vascular smooth muscle cells (VSMC)...
Sphingosine-1-phosphate (S-1-P) is a bioactive sphingolipid released from activated platelets that stimulates migration of vascular smooth muscle cells (VSMC) in vitro. S-1-P will activate akt, which can regulate multiple cellular functions including cell migration. Akt activation is downstream of phosphatidylinositol 3′-kinase (PI3-K) and phosphoinositide-dependent protein kinase-1 (PDK1). The objective...
With the rise in metabolic syndrome, understanding the role of insulin signaling within the cells of vasculature has become more important but yet remains poorly defined. This study examines the role of insulin actions on a pivotal cross-talk receptor, epidermal growth factor receptor (EGFR). EGFR is transactivated by both G-protein–coupled receptors and receptor-linked tyrosine kinases and is key...
Plasminogen activators are used routinely for thrombolysis. They lead to the generation of the protease, plasmin, which can induce smooth muscle cell proliferation and may thus promote further intimal hyperplasia in the thrombolysed vessel. We have shown recently that plasmin induces extracellular signal-regulated kinase 1/2 (ERK1/2)–mediated cell proliferation. Plasmin can also activate metalloproteinases...
Background: Intimal hyperplasia remains the leading cause of vein graft failure. Various external stenting devices have been shown to reduce the development of intimal hyperplasia in vein grafts. Mitogenic and mechanotransduction signals are known to be mediated by G protein–coupled receptors. Therefore in this study we examined the alterations in G protein expression and receptor coupling in vein...
Background: Vein graft intimal hyperplasia is associated with changes in G protein expression. The carboxyl terminus of the β-adrenergic receptor kinase-1 (β ARK CT ) is known to inhibit Gβγ-mediated mitogen–activated signaling pathways. This study examines the effects of adenoviral-mediated β ARK CT infection on the development of intimal hyperplasia in vein grafts. Methods: New Zealand...
Background: This study examines the effect of the angiotensin II receptor (type 1) antagonist (L158,809) on the formation of vein graft intimal hyperplasia in vivo, by both localized and systemic administration. Methods: Forty New Zealand White rabbits underwent right carotid interposition bypass grafting with the external jugular vein and were killed on postoperative day 28. To determine the effect...
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