Mussel adhesive protein fused with VE-cadherin domain specifically triggers endothelial cell adhesion.

Endothelium is the only known completely non-thrombogenic material. In the present study, a strategy to mimic the adhesive interactions of endothelial cells (ECs) to alter the vascular microenvironment was established and applied to directing the behaviour of cells. To facilitate the regeneration of a functional endothelium in vascular lesions, we designed a recombinant mussel foot protein (Mfp-5) fused with the VE-cadherin extracellular domain EC1-2, termed VE-M. Surface coating analysis showed that recombinant VE-M successfully formed a coating on substrate materials with uniform nanorods, low roughness, and sufficient hydrophilicity. We then evaluated the effects of VE-M on the adhesion of ECs and the capture of endothelial progenitor cells (EPCs). The result demonstrated that VE-M efficiently promoted the adhesion of ECs and EPCs. The number of ECs and EPCs on VE-M was 5.5- and 1.8-fold higher, respectively, than that on bare 316L SS under static conditions, whereas there was no significant difference in the number of captured smooth muscle cells (SMCs) between VE-M and other substrates. In addition, the number of EPCs captured by VE-M was approximately four times higher than that captured by 316L SS under dynamic conditions. In particular, the result of the neutralization test indicated that VE-M specifically triggered ECs' adhesion via the interaction of VE-cadherin EC1-2. Further investigation showed that VE-M significantly increased the levels of endogenous VE-cadherin in HUVECs as well as the endothelial eNOS content, with little or no endothelial inflammation. Our results showed that VE-M could be a promising biomimetic modification for accelerating endothelialization and vascularization in tissue engineering.