Mammalian cells are promising agents for cell therapy, diagnostics, and drug delivery. For full utilization of the cells, development of an exoskeleton may be beneficial to protecting the cells against the environmental stresses and cytotoxins to which they are susceptible. We report here a rapid single-step method for growing metal–organic framework (MOF) exoskeletons on a mammalian cell surface under cytocompatible conditions. The MOF exoskeleton coating on the mammalian cells was developed via a one-pot biomimetic mineralization process. With the exoskeleton on, the individual cells were successfully protected against cell protease (i.e., Proteinase K), whereas smaller-sized nutrient transport across the exoskeleton was maintained. Moreover, vital cellular activities mediated by transmembrane GLUT transporter proteins were also unaffected by the MOF exoskeleton formation on the cell surfaces. Altogether, this ability to control the access of specific molecules to a single cell through the porous exoskeleton, along with the cytoprotection provided, should be valuable for biomedical applications of mammalian cells.
A facile synthesis of apatite nanocrystals analogous to bioapatites with increased biocompatibility and biodegradability can remedy the shortcomings of the widely applied synthetic hydroxyapatite (HAp) for bone defect treatment. Here, we propose an expeditious synthesis method to develop a biomimetic B-type carbonate apatite (CAp) with a simple capillary microfluidic device at room temperature. The process not only eliminates fluctuations with the addition of carbonate but also produces safe CAp drug carriers through simultaneous alendronate incorporation to the CAp structure. CAp displayed superior mineralization on osteoblast-like MG-63 cells when compared with HAp and HAp drug carriers that were produced using identical methods. Furthermore, alendronate-incorporated CAp drug carriers potentially displayed higher cancer cell suppression when applied to breast cancer cells attached to the bone tissue model, which signifies enhanced cancer metastasis to bone suppression due to the likelihood of increased alendronate release of CAp owing to its faster dissolution. Overall, our results may provide promising opportunities for enhanced clinical CAp application for bone defect treatment, particularly for bone loss and cancer to bone metastasis.
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