Improvement in endothelial cell adhesion and retention under physiological shear stress using a laminin-apatite composite layer on titanium.

Apatite (Ap), laminin-apatite composite (L5Ap, L10Ap, L20Ap and L40Ap) and albumin-apatite (AlbAp) composite layers were prepared on titanium (Ti) using a supersaturated calcium phosphate solution supplemented with laminin (0, 5, 10, 20 and 40 µg ml(-1)) or albumin (800 µg ml(-1)). With an increase in the concentrations of laminin in the supersaturated calcium phosphate solutions, the amounts of laminin immobilized on the Ti increased. The number of human umbilical vein endothelial cells (HUVECs) adhered to the laminin-apatite composite layers were remarkably higher than those to the untreated Ti, Ap layer and AlbAp composite layer. The number of cells adhered to the L40Ap was 4.3 times the untreated Ti. Moreover, cells adhered to the laminin-apatite composite layers showed significantly higher cell retention under the physiological shear stress for 1 h and 2 h than those to the untreated Ti, Ap layer and AlbAp composite layer. The number of cells remaining on the L40Ap under the physiological shear stress for 2 h was 9.5 times that of the untreated Ti. The laminin-apatite composite layer is a promising interfacial layer for endothelialization of blood-contacting materials.

Tissue-engineered endothelial cell layers on surface-modified Ti for inhibiting in vitro platelet adhesion.

A tissue-engineered endothelial layer was prepared by culturing endothelial cells on a fibroblast growth factor-2 (FGF-2)-l-ascorbic acid phosphate magnesium salt n-hydrate (AsMg)-apatite (Ap) coated titanium plate. The FGF-2-AsMg-Ap coated Ti plate was prepared by immersing a Ti plate in supersaturated calcium phosphate solutions supplemented with FGF-2 and AsMg. The FGF-2-AsMg-Ap layer on the Ti plate accelerated proliferation of human umbilical vein endothelial cells (HUVECs), and showed slightly higher, but not statistically significant, nitric oxide release from HUVECs than on as-prepared Ti. The endothelial layer maintained proper function of the endothelial cells and markedly inhibited in vitro platelet adhesion. The tissue-engineered endothelial layer formed on the FGF-2-AsMg-Ap layer is promising for ameliorating platelet activation and thrombus formation on cardiovascular implants.