A Polymeric Strategy Empowering Vascular Cell Selectivity and Potential Application Superior to Extracellular Matrix Peptides

Endothelialization of vascular implants plays a vital role in maintaining the long-term vascular patency. In situ endothelialization and re-endothelialization is generally achieved by selectively promoting endothelial cell (EC) adhesion and, meanwhile, suppressing smooth muscle cell (SMC) adhesion. Currently, such EC versus SMC selectivity is achieved and extensively used in vascular-related biomaterials utilizing extracellular-matrix-derived EC-selective peptides, dominantly REDV and YIGSR. Nevertheless, the application of EC-selective peptides is limited due to their easy proteolysis, time-consuming synthesis, and expensiveness. To address these limitations, a polymeric strategy in designing and finding EC-selective biomaterials using amphiphilic beta-peptide polymers by tuning serum protein adsorption is reported. The optimal beta-peptide polymer displays EC versus SMC selectivity even superior to EC-selective REDV peptide regarding cell adhesion, proliferation, and migration of ECs versus SMCs. Study of the mechanism indicates that surface adsorption of bovine serum albumin, an abundant and anti-adhesive serum protein, plays a critical role in the ECs versus SMCs selectivity of beta-peptide polymer. In addition, surface modification of the optimal beta-peptide polymer effectively promotes the endothelialization of vascular implants and inhibits intimal hyperplasia. This study provides an alternative strategy in designing and finding EC-selective biomaterials, implying great potential in the vascular-related biomaterial study and application.

Automated summary

This study reports a polymeric strategy for designing and finding endothelial cell (EC)-selective biomaterials by tuning serum protein adsorption. The optimal beta-peptide polymer shows superior EC versus smooth muscle cell (SMC) selectivity compared to the commonly used EC-selective peptides. Surface adsorption of bovine serum albumin plays a critical role in the selectivity of the beta-peptide polymer. Surface modification of the optimal polymer promotes the endothelialization of vascular implants and inhibits intimal hyperplasia.