Literature DB >> 18831592

Biofunctionalization of biomaterials for accelerated in situ endothelialization: a review.

Achala de Mel1, Gavin Jell, Molly M Stevens, Alexander M Seifalian.   

Abstract

The higher patency rates of cardiovascular implants, including vascular bypass grafts, stents, and heart valves are related to their ability to inhibit thrombosis, intimal hyperplasia, and calcification. In native tissue, the endothelium plays a major role in inhibiting these processes. Various bioengineering research strategies thereby aspire to induce endothelialization of graft surfaces either prior to implantation or by accelerating in situ graft endothelialization. This article reviews potential bioresponsive molecular components that can be incorporated into (and/or released from) biomaterial surfaces to obtain accelerated in situ endothelialization of vascular grafts. These molecules could promote in situ endothelialization by the mobilization of endothelial progenitor cells (EPC) from the bone marrow, encouraging cell-specific adhesion (endothelial cells (EC) and/or EPC) to the graft and, once attached, by controlling the proliferation and differentiation of these cells. EC and EPC interactions with the extracellular matrix continue to be a principal source of inspiration for material biofunctionalization, and therefore, the latest developments in understanding these interactions will be discussed.

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Year:  2008        PMID: 18831592     DOI: 10.1021/bm800681k

Source DB:  PubMed          Journal:  Biomacromolecules        ISSN: 1525-7797            Impact factor:   6.988


  54 in total

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4.  Nitric oxide-eluting nanocomposite for cardiovascular implants.

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5.  Bioclickable and mussel adhesive peptide mimics for engineering vascular stent surfaces.

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Review 8.  Biomaterials to prevascularize engineered tissues.

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9.  Spreading, proliferation and differentiation of human dental pulp stem cells on chitosan scaffolds immobilized with RGD or fibronectin.

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10.  Chemical activation and changes in surface morphology of poly(ε-caprolactone) modulate VEGF responsiveness of human endothelial cells.

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