Angiogenic methacrylic acid copolymers adsorb different proteins and result in lower complement activation in comparison to poly (methyl methacrylate)

摘要

Numerous complement proteins adsorbed onto 45% MAA beads and had minimal complement activation, as measured by C3a and SC5b9 activity. Conversely. PMMA beads primarily adsorbed common proteins such as apolipoprotein. albumin, and fibrinogen, and had significantly higher complement activation. The adsorbed C1q. C3 and C4 could have caused a decrease in complement activation or the adsorbed factor H could have increased complement inhibition. Studies show that lower complement activation reduces fibrotic responses to biomaterials. Furthermore, the binding of C1q to HUVEC has been shown to modulate cell behavior to potentially promote angiogenesis. Therefore, complement inhibition is likely one mechanism contributing to the MAA-driven angiogenesis seen in previous studies. While these in vitro studies used fresh serum to preserve complement protein activity, they do not include biological observations with cells or an in vivo wound healing environment. Therefore, future studies will focus on cell studies using complement inhibitors and on mouse models that include and exclude relevant complement factors to determine the impact of complement activation and inhibition on biological responses to 45% MAA.