T5 - Modeling Magnesium Surface Protein Adhesion to Assess Hemocompatibility

Saturday, October 11, 2025

10:00 AM - 11:00 AM PDT

Location: Exhibit Hall F, G & H

Presenting Author(s)

Araylia-Marie L. Martinez

Biomedical Engineering Research Intern
Oregon Health and Science University, Clark College
Battleground, Washington, United States

Co-Author(s)

CB

Cole Baker, BS

Student
Oregon Health & Science University, United States
CK

Catie King

Biomedical Engineering Research Intern
Oregon Health and Science University, University of Wisconsin-Madison, United States
Deirdre Anderson

Scientist
Oregon Health & Science University
Portland, Oregon, United States

Primary Investigator(s)

MH

Monica Hinds

Professor
Oregon Health & Science University, United States

Introduction: : Cardiovascular stents are surgical implants, used to cardiovascular disease patients, that are placed into arteries to preserve blood flow to the heart. Within the US, 434,230 cases of Percutaneous Coronary Intervention were reported in the past year [1]. Bare-metal stents (BMS) and drug-eluting stents (DES) are currently used to treat patients that have restricted circulation based on narrowing arteries [2]. However, there are many causes of failure for these devices. Common risks associated with commercial stents include inflammation, stent thrombosis, restenosis, or bleeding due to anti-platelet therapies[2]. Bioresorbable stents (BRS) are an advancement due to their ability to preserve patency and dissolve over time before causing long lasting health risks[2]. Previous research conducted within our laboratory found that magnesium-based stents have the reduced platelet deposition rates compared to other BMS materials and clinical controls[3]. Currently, the mechanism of this decreased platelet attachment is unknown. I hypothesized that the reduced platelet deposition is due to reductions in protein adsorption on the magnesium surface. Characterizing magnesium’s surface properties, specifically involving how proteins in the bloodstream interact with the metal, are necessary to understand the biocompatibility of the potential BRS material. This study quantifies the coagulation cascade protein fibrinogen’s adhesion to the surface of magnesium materials to study how protein in the bloodstream might similarly react to magnesium BRS.

Materials and

Methods: : Sourcing of the magnesium (99.9%) and stainless steel rods (5 mm diameter) were from Goodfellow® and Fort Wayne Metals Research Products®. Polyethylenimine (PEI) coated glass slides (5 mm diameter) were used as a positive control for protein adhesion. PEI coating was done with 1%, PEI in milli-q water. Slides were created with regular glass slides that were incubated in the PEI solution overnight prior to the experiment. Fluorescent fibrinogen stock was created with 2 mg/mL stock in PBS. Working solutions for experiments utilized 1 mg/mL concentrations. Rods were sonicated in a 1510 Ultrasonic Cleaner (Branson®) for 15 minutes. Each sample was washed with PBS three times, placed into individual 0.6 mL tubes and submerged in 200 uL of the fibrinogen solution. Tubes were placed in a 37 ℃ incubator (Jeio®) on a nutating mixer(Thermo Fisher Scientific®) for one hour. After incubation, the samples were washed with PBS three times to remove any loose proteins and placed into separate wells of a 96 well black fluorescent plate (Corning®). An Infinite® M Plex (TECAN®) was utilized with fluorescence recorded at excitation 488 and emission 520. PEI coated glass samples were imaged under an Eclipse TE2000 Inverted Microscope (Nikon®) to collect representative images to confirm the presence of fluorescent fibrinogen in each sample. Fluorescent quantitation was analyzed with one-way ANOVA and post-hoc Turkey test to assess significance.

Results, Conclusions, and Discussions:: While magnesium was anticipated to have lower rates of fibrinogen adhesion, the results indicate that this hypothesis was false. Data supports the conclusion that magnesium does not limit protein deposition, represented by the increased amount of fluorescent fibrinogen found in the fluorescent detection plate reading compared to controls. Prior work in our lab demonstrated reduced thrombogenicity of magnesium materials, however, fibrinogen deposition was higher on magnesium material[3]. This indicates magnesium-based materials reduce thrombosis through a separate mechanism unrelated to fibrinogen adsorption. Reduced thrombosis may be caused by an increased amount of corrosion byproducts that affect specific parts of the coagulation cascade, rather than an overall reduction in protein deposition. In conclusion, magnesium has unexpectedly been observed to have a higher amount of fibrinogen deposition but still retains its anti-thrombogenic properties ex vivo[3]. The relationship between protein deposition, magnesium byproducts, and thrombogenesis needs to be characterized further to determine the implications this may cause for surgical implants and patient health. Additional research to develop an understanding of magnesium’s surface properties and associated mechanisms regarding hemocompatibility is necessary to create informed decisions for optimizing material design best suited for biodegrading stents.

Acknowledgements and/or References (Optional): : [1] S. Martin, et al. "2024 Heart Disease and Stroke Statistics: A Report of US and Global
Data From The American Heart Association", Circulation, 149(8), pp. 902, Feb. 2024.
https://doi.org/10.1161/cir.0000000000001209.
[2] S. Borhani, et al. “Cardiovascular stents: overview, evolution, and next generation”.
Progress in Biomaterials, 7(3), pp. 175-176, Sept. 2018.
https://doi.org/10.1007/s40204-018-0097-y.
[3] D. Anderson, et al. “Thrombogenicity of biodegradable metals.” Bioactive materials,
38(2024), pp. 411-421, May. 2024. https://doi.org/10.1016/j.bioactmat.2024.05.002.
[4] “Biodegradable Stents Market”. Transparency Market Research (2024).
https://www.transparencymarketresearch.com/biodegradable-stents-market.html
(accessed July 11, 2025).