Effects of colchicine and vinblastine on platelet contractility and release

Kuntamukkula, M.S.; Moake, JL; McIntire, Larry V.; Cimo, Philip L.

doi:10.1016/0049-3848(82)90251-1

Cited by 9 publications

(5 citation statements)

References 16 publications

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“…Other investigators, however, have reported inhibitory effects (94,95). (ii) The microtubule inhibitors, colchicine, vinblastine and vincristine disrupt the microtubules, but, according to Dr. Liischer, have no effect on shape change, fibrinogen binding, or aggregation, and little effect on the release reaction (96,97). (iii) Inhibitors of calmodulin (tri fluoperazine, chlorpromazine, W7 (N-[6 aminohexyl-5-chloro-lnaphthalene sulfonamide]) interfere with the action of light chain kinase as well as many other Ca2+-dependent processes (10,14,(98)(99)(100).…”

Section: Inhibitors O F Cytoskeletal Activitymentioning

confidence: 99%

Platelet Function Inhibitors

Packham

1983

Thromb Haemost

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Section: Inhibitors O F Cytoskeletal Activitymentioning

confidence: 99%

Platelet Function Inhibitors

Packham

1983

Thromb Haemost

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“…Colchicine decreased CRP-XL-stimulated P-selectin expression and trended toward a decrease in GPIIb/IIIa conformational change. A previous study also reported on the inhibitory effects of colchicine on collagen-mediated serotonin release from platelets ( 59 ).…”

Section: Colchicine Inhibits Collagen Mediated Platelet Activationmentioning

confidence: 82%

Perspective: Collagen induced platelet activation via the GPVI receptor as a primary target of colchicine in cardiovascular disease

Pennings

Reddel²,

Chen³

et al. 2023

Front. Cardiovasc. Med.

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Colchicine has been demonstrated to reduce cardiovascular death, myocardial infarction (MI), ischemic stroke, and ischemia-driven coronary revascularization in people with coronary artery disease (CAD). These reductions were observed even in patients already taking antiplatelet therapy. As well as having anti-inflammatory effects, colchicine demonstrates antiplatelet effects. We propose that colchicine's antiplatelet effects primarily target collagen-induced platelet activation via the collagen receptor, glycoprotein (GP)VI, which is critical for arterial thrombosis formation. In settings such as stroke and MI, GPVI signaling is upregulated. We have demonstrated in vitro that therapeutic concentrations of colchicine lead to a decrease in collagen-induced platelet aggregation and alter GPVI signaling. Clinical studies of colchicine given for 6 months lead to a significant reduction in serum GPVI levels in CAD patients, which may ameliorate thrombotic risk. Future evaluation of the effects of colchicine in clinical trials should include assessment of its effects on collagen-mediated platelet activation, and consideration be given to quantifying the contribution of such antiplatelet effects additional to the known anti-inflammatory effects of colchicine.

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“…Microtubule‐interfering agents showed consistent antimitotic functions in tumour cells, whereas their effects vary vastly in platelets . For instance, colchicine disturbs microtubule assembly and inhibits platelet release, although changes in granule secretion were not observed in vinblastine‐treated platelets . An early study showed that the colchicine effect could be reversed by stabilizing platelet microtubules with D2O, which alone may enhance platelet aggregation induced by calcium ionophore .…”

Section: Discussionmentioning

confidence: 99%

Humanin analogue, HNG, inhibits platelet activation and thrombus formation by stabilizing platelet microtubules

Ren

You

et al. 2020

J Cellular Molecular Medi

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HNG, a highly potent mutant of the anti‐Alzheimer peptide‐humanin, has been shown to protect against ischaemia‐reperfusion (I/R) injury. However, the underlying mechanism related to platelet activation remains unknown. We proposed that HNG has an effect on platelet function and thrombus formation. In this study, platelet aggregation, granule secretion, clot retraction, integrin activation and adhesion under flow conditions were evaluated. In mice receiving HNG or saline, cremaster arterial thrombus formation induced by laser injury, tail bleeding time and blood loss were recorded. Platelet microtubule depolymerization was evaluated using immunofluorescence staining. Results showed that HNG inhibited platelet aggregation, P‐selectin expression, ATP release, and αIIbβ3 activation and adhesion under flow conditions. Mice receiving HNG had attenuated cremaster arterial thrombus formation, although the bleeding time was not prolonged. Moreover, HNG significantly inhibited microtubule depolymerization, enhanced tubulin acetylation in platelets stimulated by fibrinogen or microtubule depolymerization reagent, nocodazole, and inhibited AKT and ERK phosphorylation downstream of HDAC6 by collagen stimulation. Therefore, our results identified a novel role of HNG in platelet function and thrombus formation potentially through stabilizing platelet microtubules via tubulin acetylation. These findings suggest a potential benefit of HNG in the management of cardiovascular diseases.

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Effects of colchicine and vinblastine on platelet contractility and release

Cited by 9 publications

References 16 publications

Platelet Function Inhibitors

Platelet Function Inhibitors

Perspective: Collagen induced platelet activation via the GPVI receptor as a primary target of colchicine in cardiovascular disease

Humanin analogue, HNG, inhibits platelet activation and thrombus formation by stabilizing platelet microtubules

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