Key result
Non-selective alpha IIb/beta 3 antagonists and the heat shock protein p20 inhibit platelet aggregation and reduce vascular stenosis by preventing thrombus formation and suppressing smooth muscle cell proliferation.
Why the study?
Does non-selective integrin inhibition or p20 administration reduce vascular stenosis and platelet aggregation?
Does non-selective integrin inhibition or p20 administration reduce vascular stenosis and platelet aggregation?
Answers are grounded in this paper and cite their sources.
Non-selective integrin inhibition and the heat shock protein p20 may offer novel therapeutic pathways to prevent thrombus formation and vascular restenosis after percutaneous transluminal coronary angioplasty.
The long-lasting success of PTCA, a common treatment for patients with coronary artery disease, is hampered by acute reocclusion due to thrombus and by late restenosis due to smooth muscle cell (SMC) migration and proliferation. Recently potent antiplatelet agents such as inhibitors of platelet glycoprotein (GP) IIb/IIIa (alpha IIb/beta 3) have become available and are highly effective in humans. We investigated the inhibitory effects of these compounds on vascular stenosis. Administration of an RGD-containing peptide (non-selective alpha IIb/beta 3 antagonist) results in reduction of neointima, but selective alpha IIb/beta 3 antagonists have no effect. This effect is due both to an early event, which could be due to the inhibition of secretion of PDGF from activated platelets with blocked alpha IIb/beta 3, and to a late event, by interference with SMC alpha v/beta 3. Moreover, platelet adhesion via GPIb/V/IX is a trigger for thrombus formation. Inhibition of platelet adhesion results in the prevention of thrombus formation and the suppression of neointima. However, this effect was supported by the reduction of SMC proliferation. Therefore, these dual inhibitions markedly reduced vascular stenosis. Finally some low molecular mass heat shock proteins (HSPs) appear to act as molecular chaperones, but their physiological roles have not been fully elucidated. We have investigated the physiological role of p20, a kind of HSP, on platelet function. p20 inhibited platelet aggregation. Our findings may provide the basis for a novel defensive system against thrombus formation.
No takes yet. Share an insight, caveat, or question.
Hiroyuki Matsuno (2000) conducted a review in Vascular stenosis and thrombus formation. Integrin inhibitors and HSP20 was evaluated. Non-selective alpha IIb/beta 3 antagonists and the heat shock protein p20 inhibit platelet aggregation and reduce vascular stenosis by preventing thrombus formation and suppressing smooth muscle cell proliferation.
Synapse has enriched 10 related papers. Consider them for comparative context: