Keywords

collagen, nanoparticle, angioplasty, peptide, NIPAm

Presentation Type

Event

Research Abstract

Balloon angioplasty, the most prevalent non-surgical treatment for Atherosclerosis, damages the endothelial layer of the artery, baring an underlying collagenous layer, which causes platelet adhesion and activation and eventual thrombosis and intimal hyperplasia. Previous work in our lab has used a collagen-binding peptidoglycan, dermatan-sulfate-SILY (DS-SILY), that has been shown to bind to type I collagen and prevent platelet adhesion and activation. Our goal is to fabricate nanoparticle-SILY by cross-linking SILY to a poly(N-isopropylacrylamide) (NIPAm) nanoparticle instead of a DS backbone, while retaining the SILY’s high collagen binding affinity and platelet inhibition capacity observed in DS-SILY. Using a biotin-streptavidin assay, we showed that nanoparticle-SILY has a high binding affinity when applied to a collagen-coated surface, starting at a concentration of 1 mg/mL and maximized at concentrations at or above 4 mg/mL. Using dynamic light scattering, we showed that the nanoparticle-SILY maintains the thermodynamic properties characteristic of NIPAm. The ability of the particles to inhibit platelet binding and activation will be tested by using an ELISA to measure NAP-2 and PF-4 expression in platelet rich plasma applied to a collagen surface treated with nanoparticle-SILY. We expect to find that nanoparticle-SILY is able to inhibit platelet activation, as evidenced by lower levels of NAP-2 and PF-4 released. If it can be shown that nanoparticle-SILY has the capability to prevent platelet adhesion and activation, future work could explore the potential of the nanoparticles to be loaded with anti-inflammatory peptides and used for the dual purpose of targeted drug delivery and collagen shielding.

Session Track

Health

Share

COinS
 
Aug 7th, 12:00 AM

Using Collagen Binding Poly(N-Isopropylacrylamide) Nanoparticles to Prevent Intravascular Platelet Adhesion and Activation

Balloon angioplasty, the most prevalent non-surgical treatment for Atherosclerosis, damages the endothelial layer of the artery, baring an underlying collagenous layer, which causes platelet adhesion and activation and eventual thrombosis and intimal hyperplasia. Previous work in our lab has used a collagen-binding peptidoglycan, dermatan-sulfate-SILY (DS-SILY), that has been shown to bind to type I collagen and prevent platelet adhesion and activation. Our goal is to fabricate nanoparticle-SILY by cross-linking SILY to a poly(N-isopropylacrylamide) (NIPAm) nanoparticle instead of a DS backbone, while retaining the SILY’s high collagen binding affinity and platelet inhibition capacity observed in DS-SILY. Using a biotin-streptavidin assay, we showed that nanoparticle-SILY has a high binding affinity when applied to a collagen-coated surface, starting at a concentration of 1 mg/mL and maximized at concentrations at or above 4 mg/mL. Using dynamic light scattering, we showed that the nanoparticle-SILY maintains the thermodynamic properties characteristic of NIPAm. The ability of the particles to inhibit platelet binding and activation will be tested by using an ELISA to measure NAP-2 and PF-4 expression in platelet rich plasma applied to a collagen surface treated with nanoparticle-SILY. We expect to find that nanoparticle-SILY is able to inhibit platelet activation, as evidenced by lower levels of NAP-2 and PF-4 released. If it can be shown that nanoparticle-SILY has the capability to prevent platelet adhesion and activation, future work could explore the potential of the nanoparticles to be loaded with anti-inflammatory peptides and used for the dual purpose of targeted drug delivery and collagen shielding.