Nitric oxide producing coating mimicking endothelium function for multifunctional vascular stents

Area of Science:

• Biomaterials Science
• Cardiovascular Research
• Nanotechnology

Background:

• Endothelial nitric oxide (NO) release is crucial for cardiovascular homeostasis, inhibiting platelet aggregation and smooth muscle cell proliferation.
• Vascular stents often trigger adverse responses, including restenosis, due to impaired endothelial function.
• Developing biomimetic coatings is essential to enhance stent hemocompatibility and reduce complications.

Purpose of the Study:

• To create a NO-catalytic bioactive coating that mimics the natural endothelium's function.
• To evaluate the hemocompatibility and efficacy of this coating for vascular stent applications.
• To investigate the coating's ability to prevent restenosis by modulating cellular responses.

Main Methods:

• Covalent conjugation of 3,3-diselenodipropionic acid (SeDPA) with glutathione peroxidase (GPx)-like activity to a plasma polymerized allylamine (PPAam) surface.
• Characterization of the NO-generating capability from S-nitrosothiols (RSNOs).
• In vitro assessment of platelet activation, smooth muscle cell behavior, and endothelial cell responses; in vivo evaluation of re-endothelialization and restenosis in stents.

Main Results:

• The SeDPA-PPAam coating demonstrated long-term, continuous NO generation.
• Generated NO significantly increased cGMP synthesis in platelets and smooth muscle cells.
• The coating suppressed platelet activation/aggregation and vascular smooth muscle cell adhesion/proliferation/migration.
• Enhanced adhesion, proliferation, and migration of human umbilical vein endothelial cells (HUVECs) were observed.
• In vivo studies showed promoted re-endothelialization and reduced restenosis.

Conclusions:

• The NO-catalytic bioactive coating effectively mimics endothelial NO production.
• This biomimetic coating shows significant potential to improve vascular stent biocompatibility and reduce restenosis.
• The coating promotes a favorable cellular microenvironment for enhanced re-endothelialization.