Combining Sandblasting, Alkaline Etching, and Collagen Immobilization to Promote Cell Growth on Biomedical Titanium Implants

Our objective in this study was to promote the growth of bone cells on biomedical titanium (Ti) implant surfaces via surface modification involving sandblasting, alkaline etching, and type I collagen immobilization using the natural cross-linker genipin. The resulting surface was characterized in terms topography, roughness, wettability, and functional groups, respectively using field emission scanning electron microscopy, 3D profilometry, and attenuated total reflection-Fourier transform infrared spectroscopy. We then evaluated the adhesion, proliferation, initial differentiation, and mineralization of human bone marrow mesenchymal stem cells (hMSCs). Results show that sandblasting treatment greatly enhanced surface roughness to promote cell adhesion and proliferation and that the immobilization of type I collagen using genipin enhanced initial cell differentiation as well as mineralization in the extracellular matrix of hMSCs. Interestingly, the nano/submicro-scale pore network and/or hydrophilic features on sandblasted rough Ti surfaces were insufficient to promote cell growth. However, the combination of all proposed surface treatments produced ideal surface characteristics suited to Ti implant applications.

Collagen immobilization on ultra-thin nanofiber membrane to promote in vitro endothelial monolayer formation

The endothelialization on the poly (ε-caprolactone) nanofiber has been limited due to its low hydrophilicity. The aim of this study was to immobilize collagen on an ultra-thin poly (ε-caprolactone) nanofiber membrane without altering the nanofiber structure and maintaining the endothelial cell homeostasis on it. We immobilized collagen on the poly (ε-caprolactone) nanofiber using hydrolysis by NaOH treatment and 1-ethyl-3-(3-dimethylaminopropyl) carbodiimide/sulfo- N-hydroxysulfosuccinimide reaction as a cost-effective and stable approach. NaOH was first applied to render the poly (ε-caprolactone) nanofiber hydrophilic. Subsequently, collagen was immobilized on the surface of the poly (ε-caprolactone) nanofibers using 1-ethyl-3-(3-dimethylaminopropyl) carbodiimide/sulfo- N-hydroxysulfosuccinimide. Scanning electron microscopy, Fourier transform infrared spectroscopy, transmission electron microscopy, and fluorescence microscopy were used to verify stable collagen immobilization on the surface of the poly (ε-caprolactone) nanofibers and the maintenance of the original structure of poly (ε-caprolactone) nanofibers. Furthermore, human endothelial cells were cultured on the collagen-immobilized poly (ε-caprolactone) nanofiber membrane and expressed tight junction proteins with the increase in transendothelial electrical resistance, which demonstrated the maintenance of the endothelial cell homeostasis on the collagen-immobilized-poly (ε-caprolactone) nanofiber membrane. Thus, we expected that this process would be promising for maintaining cell homeostasis on the ultra-thin poly (ε-caprolactone) nanofiber scaffolds.