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Turbidimetry on Human Washed Platelets: The Effect of the Pannexin1-inhibitor Brilliant Blue FCF on Collagen-induced Aggregation
Published on: April 6, 2017
Prevention of Collagen-Induced Platelet Binding and Activation by Thermosensitive Nanoparticles
James McMasters1, Alyssa Panitch
1Weldon School of Biomedical Engineering, Purdue University, 206 S. Martin Jischke Dr., West Lafayette, Indiana, 47907, USA.
Insights
Researchers developed novel collagen-binding nanoparticles to prevent platelet activation after angioplasty. These nanoparticles reduce inflammation and offer potential for targeted drug delivery to damaged vasculature.
Area of Science:
- Biomaterials Science
- Nanotechnology
- Vascular Biology
Background:
- Peripheral artery disease (PAD) involves atherosclerotic blockages in peripheral arteries, often treated with angioplasty.
- Angioplasty can damage the vascular endothelium, exposing collagen and activating platelets, leading to restenosis.
- Current treatments lack targeted approaches to mitigate post-angioplasty inflammation and restenosis.
Purpose of the Study:
- To develop novel nanoparticles capable of binding exposed collagen.
- To investigate the nanoparticles' ability to inhibit collagen-mediated platelet activation.
- To assess the nanoparticles' potential as a drug delivery platform for anti-inflammatory agents.
Main Methods:
- Synthesis of poly(NIPAm-MBA-AMPS-AAc) nanoparticles with surface-conjugated collagen I-binding peptides.
- Assessment of nanoparticle binding to collagen I-coated surfaces using binding assays.
- Evaluation of platelet activation inhibition via collagen-mediated pathways.
- Characterization of nanoparticle properties including temperature sensitivity, colloidal stability, and drug loading/release capacity.
Main Results:
- Nanoparticles demonstrated binding to collagen I at concentrations above 0.5 mg/mL.
- These nanoparticles inhibited collagen-mediated platelet activation by over 60%.
- The nanoparticles exhibited temperature sensitivity and colloidal stability, suitable for drug delivery, and could load/release anti-inflammatory peptides.
Conclusions:
- Developed collagen-binding nanoparticles offer a dual therapeutic approach for PAD.
- These nanoparticles can prevent collagen-mediated platelet activation and deliver therapeutics to damaged vasculature.
- This technology holds promise for reducing restenosis after angioplasty and improving PAD treatment outcomes.
Abstract:
Peripheral artery disease is an atherosclerotic occlusion in the peripheral vasculature that is typically treated via percutaneous transluminal angioplasty. Unfortunately, deployment of the angioplasty balloon damages the endothelial layer, exposing the underlying collagen and allowing for the binding and activation of circulating platelets, which initiate an inflammatory cascade leading to eventual restenosis. Here, we report on the development of poly(NIPAm-MBA-AMPS-AAc) nanoparticles that have a collagen I-binding peptide crosslinked to their surface allowing them to bind to exposed collagen. Once bound, these particles mask the exposed collagen from circulating platelets, effectively reducing collagen-mediated platelet activation. Using collagen I-coated plates, we demonstrate that these particles are able to bind to collagen at concentrations above 0.5 mg/mL. Once bound, these particles inhibit collagen-mediated platelet activation by over 60%. Using light scattering and zeta potential measurements, we investigated the potential of the nanoparticles as a drug delivery platform. We have verified that the collagen-binding nanoparticles retain the temperature sensitivity common to poly(NIPAm)-based nanoparticles while remaining colloidally stable in aqueous environments. We also demonstrate that they are able to passively load and release anti-inflammatory cell penetrating peptides. Combined, we have developed a collagen-binding nanoparticle that has dual therapy potential, preventing collagen-mediated platelet activation while delivering water-soluble therapeutics directly to the damaged area.
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