Highlights d Ultrasound-induced neuromodulation is initiated by opening of TRPA1 in astrocytes d The Ca 2+ entry through TRPA1 causes a release of glutamate through Best1 channels d The released glutamate activates NMDA receptors in neighboring neurons
Intravenous administration
of mesenchymal stem cells (MSCs) has
served as a clinical intervention for inflammatory diseases. Once
entered to blood circulation, MSCs are exposed to a harsh environment
which sharply decreases cell viability due to the fact that injected
cells, being susceptible to shear stress, are subjected to the high
velocities of the bloodstream and lack of proper mechanical support
that keeping them in an attachment-deprived state. Here, we coated the nanofilm onto viable
MSCs by depositing poly-l-lysine and hyaluronic acid molecules
along with arginine-glycine-aspartic acid (RGD peptide) as building
blocks to protect cells from shear stress and stabilize them in a
single cell, suspension state. In this article, we found that nanofilm-coated
cells showed significantly increased cell survival in vitro and in vivo, which was also supported by the activation
of survival-related protein, Akt. The coated nanofilm did not interfere
with the stemness of MSCs which was determined based on the colony
forming unit-fibroblast (CFU-F) assay and in vitro differentiation potential. Because of the characteristics of films
showing light molecular deposition density, flexibility, and looseness,
application of nanofilms did not block cell migration. When the cells
were administrated intravenously, the nanofilm coated MSCs not only
prolonged blood circulation lifetime but also showed increased stem
cell recruitment to injured tissues in the muscle injury in
vivo model, due to prolonged survival. Surface modification
of MSCs using nanofilms successfully modulated cell activity enabling
them to survive the anoikis-inducing state, and this can provide a
valuable tool to potentiate the efficacy of MSCs for in vivo cell therapy.
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